Prospective studies found associations between serum uric acid (SUA) and incident metabolic syndrome (MetS) with high heterogeneity. We investigated the association between SUA and incident MetS and its components in a region highly burdened by cardiometabolic disorders.

The study included 1999 adults (1297 women). MetS was defined according to the Joint Interim Societies' criteria. Multivariate adjusted Cox proportional hazard analyses were applied to examine the association between SUA and outcomes. During a median follow-up of 9.7 years, 833 (510 women) incident MetS cases occurred. Among the whole population, a higher risk of MetS was observed across quartiles (Q1-4) of SUA even after adjustment for Homeostasis Model Assessment for Insulin Resistance (HOMA-IR), [multivariate hazard ratio (95 % confidence interval) in Q4: 1.58 (1.17-2.14), Q1: as reference]. Generally, same association was found for women. Similarly, a 1-standard deviation (SD) increase of SUA was associated with a higher risk of incident MetS in the whole population, and women [1.19 (1.06-1.34) and 1.14 (1.02-1.28), respectively]. Among men, the association was just in the age-adjusted analysis, however, no effect modification of gender was found. Moreover, a 1-SD increase in SUA elevated the risk of incident high-waist circumference (20 %), -fasting plasma glucose (19 %), -triglycerides (17 %), and low-high-density lipoprotein cholesterol (12 %) after adjustment for other MetS components and HOMA-IR in the whole population (all Ps < 0.05).

SUA was associated with incident MetS and its components, excluding hypertension, and might be a potential biomarker for identifying individuals at risk of developing MetS.

The link between oxidative stress and lipid metabolism is widely studied, but their causal relationship in the general population remains unclear.

We utilized weighted regression and propensity score matching (PSM) models to investigate the relationship between endogenous oxidative stress markers (serum bilirubin and uric acid) and lipid metabolism in 11,087 participants of European ancestry from the National Health and Nutrition Examination Survey (NHANES) during the period from 2005 to 2018. Additionally, we performed a bidirectional two-sample Mendelian randomization (MR) analysis using Genome-Wide Association Study (GWAS) summary statistics from individuals of European ancestry (n = 997 to 575,531) to explore the genetic causal relationship between oxidative stress markers and lipid metabolism profiles (n = 20,430).

Weighted regression showed that serum uric acid significantly increased high cholesterol (OR = 1.11, 95 % CI = 1.06-1.15, P < 0.001) and high triglycerides (OR = 1.25, 95 % CI = 1.20-1.30, P < 0.001). PSM analysis confirmed that serum uric acid increased the incidence of high triglycerides (OR = 1.57, 95 % CI = 1.35-1.82, P < 0.001). Additionally, a strong bidirectional genetic relationship was found between oxidative stress markers and lipid metabolism. For example, serum uric acid increased serum triglycerides (β = 0.1904, Se = 0.05, P < 0.001) and decreased total cholesterol in very large HDL (β = -0.1298, Se = 0.039, P < 0.001). Conversely, total cholesterol reduced direct bilirubin levels (β = -0.1707, Se = 0.018, P < 0.001). No significant horizontal pleiotropy was detected by MR-Egger intercept.

Our findings demonstrate a robust genetic and population-based association between oxidative stress markers and lipid metabolism, suggesting potential therapeutic targets for lipid disorders based on endogenous oxidative stressors.

Acrylamide (AA) has raised concerns throughout the world in recent years because of its potential negative effects on human health. Numerous researches on humans and animals have connected a high dietary exposure to AA to a possible risk of cancer. Additionally, higher consumption of acrylamide has also been associated with dysfunctioning of various organ systems from nervous system to the reproductive system. Acrylamide is primarily metabolised into the glycidamide inside the body which gets accumulated in different tissues including kidney and liver, and chronic exposure to this can lead to the nephrotoxicity and hepatotoxicity through different molecular mechanisms. This review summarizes the various sources, formation and metabolism of the dietary acrylamide along with the different molecular mechanisms such as oxidative stress, inflammation, DNA damage, autophagy, mitochondrial dysfunction and morphological changes in nephron and hepatocytes through which acrylamide exerts its deleterious effect on kidney and liver causing nephrotoxicity and hepatotoxicity. This review summarizes various animal and cellular studies that demonstrate AA-induced nephrotoxicity and hepatotoxicity. Lastly, the article emphasizes on underlying protective molecular mechanisms of various pharmacological interventions against acrylamide induced hepatotoxicity and nephrotoxicity.

The intricate linking between the health of blood vessels and the functioning of neurons has attracted growing attention in the context of disorders that affect the neurological environment. Endothelial cells, forming the blood-brain barrier and blood-retinal barrier, play a fundamental role in maintaining the integrity of the brain-retina microenvironment connection. This review explores the molecular foundations of endothelial cell dysfunction and its implications for the brain-retina interaction. A comprehensive analysis of the complex factors contributing to endothelial dysfunction is presented, including oxidative stress, inflammation, reduced nitric oxide signaling, and disrupted vascular autoregulation. The significance of endothelial dysfunction extends to neurovascular coupling, synaptic plasticity, and trophic support. To our knowledge, there is currently no existing literature review addressing endothelial microvascular dysfunction and its interplay with the brain-retina microenvironment. The review also explains bidirectional communication between the brain and retina, highlighting how compromised endothelial function can disrupt this vital crosstalk and inhibit normal physiological processes. As neurodegenerative diseases frequently exhibit vascular involvement, a deeper comprehension of the interaction between endothelial cells and neural tissue holds promise for innovative therapeutic strategies. By targeting endothelial dysfunction, we may enhance our ability to preserve the intricate dynamics of the brain-retina microenvironment connection and ameliorate the progression of neurological disorders.

Alzheimer's disease (AD) is increasingly recognized as a systemic disorder with a substantial metabolic disorder component, where the liver significantly impacts the brain via the liver-brain axis. Key mechanisms include the liver's role in clearing peripheral β-amyloid (Aβ), the influence of hepatic enzymes and metabolites on cognitive decline, and the systemic effects of metabolic disorders on AD progression. Hepatokines, liver-secreted proteins including fibroblast growth factor (FGF)-21, selenoprotein P (SELENOP), Fetuin-A, Midbrain astrocyte-derived neurotrophic factor (MANF), apolipoprotein J (ApoJ), sex hormone-binding globulin (SHBG), Adropin and Angiopoietin-like protein 3 (ANGPTL3), could regulate insulin sensitivity, lipid metabolism, oxidative stress, immune responses, and neurotrophic support. These pathways are closely linked to core AD pathologies, including Aβ aggregation, tau hyperphosphorylation, neuroinflammation, oxidative stress and mitochondrial dysfunction. Lifestyle interventions, including exercise and dietary modifications, that regulate hepatokines expression may offer novel preventive and therapeutic strategies for AD. This review synthesizes current knowledge on the liver-brain crosstalk in AD, emphasizing the mechanistic role of liver in bridging metabolic dysfunction with neurodegeneration and underscores the diagnostic and therapeutic potential of hepatokines in addressing AD's complex pathology.

The fat-to-muscle mass ratio (FMR) has served as a marker for various diseases. This study aimed to explore sex-specific associations between FMR in different body regions (whole body, trunk, arm, and leg) and cancer incidence.

We included 435,986 cancer-free participants (203,133 men and 232,853 women) from the UK Biobank at baseline. FMR was calculated as the ratio of fat mass to muscle mass in each body region. Multivariable Cox proportional hazards models, along with Cox models incorporating restricted cubic splines (RCS) function, were employed to examine both linear and non-linear associations between FMR and cancer risk in men and women. Additionally, a combined grouping of body mass index (BMI) and FMR was used to assess the joint impact of body composition on cancer incidence.

During the follow-up period, 62,060 new cancer cases were recorded. Our analysis showed significant associations between both total and regional FMR and the risk of several cancers. In men, higher whole body FMR was associated with an increased risk of esophagus, stomach, colorectal, liver, pancreas, and kidney cancers, while a decreased risk was observed for prostate and non-melanoma skin cancers (FDR < 0.05). In women, higher FMR was associated with a higher incidence of gallbladder, pancreas, kidney, thyroid, breast, and uterus cancers (FDR < 0.05). Non-linear associations were observed for several cancer types, with specific FMR cut-off points presented using RCS curves. The analysis by combining BMI and FMR suggested potential interaction patterns, revealing some masked risks; for example, a significant increase in cancer incidence was also observed in individuals exhibiting high FMRs despite having low BMI.

Our findings suggested that both total and regional FMR may serve as potential biomarkers for assessing the risk of overall and site-specific cancers.

Lesbicoumestans are a class of bioactive compounds isolated from the roots of Lespedeza bicolor (L. bicolor). These compounds have been reported to exhibit anticancer and antiproliferative activities. In this study, our primary focus was to examine the antioxidant capabilities of lesbicoumestan (7) (LC-7), a newly isolated coumestan from roots of L. bicolor, using lipopolysaccharide (LPS)-stimulated immortalized mouse Kupffer cells (ImKCs) as the experimental model. The investigation revealed that LC-7 played a pivotal role in inhibiting the production of reactive oxygen species (ROS). Additionally, LC-7 effectively restored the imbalanced glutathione(GSH)/glutathione disulfide ratio and enhanced the activity of glutathione peroxidase (GPx) following cellular exposure to LPS. Moreover, our investigation revealed that LC-7 exhibited the capacity to enhance the expression of heme oxygenase-1 (HO-1), leading to inhibition of nitric oxide (NO) and proinflammatory cytokines production induced by LPS. Notably, LC-7 did not significantly impact the nuclear factor kappa B cells (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. Intriguingly, LC-7 modulated the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway by direct interaction with Kelch-like-ECH-associated protein 1 (Keap1). These findings suggest that LC-7 possesses antioxidant and anti-inflammatory properties in LPS-stimulated ImKCs by upregulating Nrf2 expression.

Polystyrene nanoplastics (PS-NPs) are result from the degradation of plastic and have diameters ranging from 1 nm to 100 nm. The objective of this study is to provide information on the adverse effects of PS-NPs with in vitro and in vivo analyses of liver injury. An in vitro study was conducted using confocal microscopy, flow cytometry, and MTT test analysis. An in vivo study was conducted to determine apoptosis levels, glucose metabolism gene expressions, liver enzymes, and liver histology. Data were analyzed using GraphPad Prism software 10.2.1. The in vitro study showed the absorption of PS-NPs in the cell cytoplasm, the percentage of apoptosis, 3t3, and the WiDr cell lines' viability. The in vivo analysis showed that PS-NPs can stimulate liver injuries, such as inducing the elevation of liver enzymes, necrosis, edema, inflammation, and the dilatation of the portal vein diameter. High levels of caspase-3, caspase-9, and Bax were detected, as well as the expression of several genes including PI3K, AKT, PEPCK, GLUT2, and PK. In conclusion, the in vitro analysis showed the detrimental effects of PS-NPs on cells, such as high levels of apoptosis and low cell viability, while the in vivo studies displayed the impairment of liver tissue and disturbances in glucose metabolism regulation.

Artemisia schmidtiana Maxim., a plant belonging to the Asteraceae family, is renowned for its extensive ethnomedicinal applications and distinctive aromatic qualities. This study evaluated the chemical composition, antioxidant capacity, and inhibitory effects on acetylcholinesterase (AChE), α-glucosidase, and β-lactamase of its essential oil (EO). The major constituents of the EO were identified as germacrene D (16.29%), falcarinol (11.02%), β-caryophyllene (9.43%), α-zingiberene (7.93%), phytol (6.06%), and α-humulene (4.04%). The EO demonstrated radical scavenging activity against DPPH (44.9% at 5 mg/mL) and ABTS (IC50 = 0.72 ± 0.02 mg/mL) radicals, with a FRAP antioxidant capacity of 126.61 ± 0.59 μmol·g-1. Additionally, the EO exhibited modest AChE inhibition (16.7% at 250 μg/mL) and significant inhibition of α-glucosidase and β-lactamase, with IC50 values of 178.80 ± 17.02 μg/mL and 40.06 ± 8.22 μg/mL, respectively. Molecular docking revealed favorable interactions between the major EO compounds and the tested enzymes, providing a theoretical foundation for future drug development. These findings suggest that A. schmidtiana EO holds potential for applications in the food and pharmaceutical industries, warranting further investigation.

Oxidative stress and impaired antioxidant defenses contribute significantly to liver dysfunction, particularly with aging. This study evaluated the dose- and age-dependent effects of dietary ginger (Zingiber officinale) supplementation on liver antioxidant defense systems in mice.

Male Swiss Webster mice aged 3, 6, and 12 months (n = 48 per age group) received standard feed or feed supplemented with either 0.6% or 1.8% dried ginger powder for 3 months. Liver tissue was analyzed for multiple antioxidant parameters, including DPPH radical scavenging activity, total antioxidant capacity, vitamin C levels, total phenolic content, superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, and reduced glutathione (GSH) concentrations.

The results demonstrated significant age-dependent declines in several antioxidant parameters in control animals, including DPPH scavenging activity, total antioxidant capacity, vitamin C levels, total phenolic content, and SOD activity. Ginger supplementation produced differential effects based on both dose and age. While 3-month-old mice showed decreased DPPH radical scavenging with ginger supplementation, both 6- and 12-month-old mice exhibited significantly increased activity. Higher-dose (1.8%) ginger supplementation enhanced GSH levels across all age groups, with effects being most pronounced in older mice. SOD activity remained unaffected by ginger supplementation across all groups. MDA levels were significantly reduced by 1.8% ginger supplementation in 3-month-old mice, with smaller, dose-dependent but non-significant reductions in older groups.

These findings demonstrate that ginger's effects on liver antioxidant systems are both dose- and age-dependent, with generally stronger beneficial effects observed at higher doses and in older animals. The observed dose- and age-dependent variations emphasize the importance of personalized supplementation strategies and provide a foundation for future research into the molecular mechanisms underlying ginger's antioxidant effects.

Ultra-high-performance liquid chromatography-time-of-flight mass spectrometry (UHPLC-TOF-MS) was employed to analyze serum metabolites and metabolic pathways associated with metabolic syndrome (MS) in the Yi and Han populations of Yunnan.

Participants included individuals diagnosed with MS and healthy controls from the Yi and Han populations of Yunnan. Serum nontargeted and amino acid-targeted metabolomics analyses were conducted to identify differential serum metabolites (DEMs) and metabolic pathways associated with MS pathogenesis in these two ethnic groups.

Nontargeted metabolomics analysis revealed 2,762 DEMs in the MS group of the Han population, while 1,535 DEMs were identified in the MS group of the Yi population [variable importance in projection (VIP)>1, P<0.05]. Venn analysis highlighted common and unique DEMs between the two populations. KEGG pathway analysis identified seven significantly enriched pathways in the Han group and five in the Yi group, primarily involving amino acid synthesis and metabolism. To investigate the role of amino acids in MS, serum levels of 71 endogenous amino acids were quantified. In the MS group of the Han population, 19 differential amino acids were identified, significantly enriched in pathways related to D-glutamine and D-glutamate metabolism, as well as cysteine and methionine metabolism. In the Yi population, six differential amino acids were identified, with significant enrichment in D-glutamine and D-glutamate metabolism, sulfur metabolism, and valine, leucine, and isoleucine biosynthesis.

Our study investigates metabolic differences in metabolic syndrome (MS) between Yi and Han populations through nontargeted and targeted metabolomics approaches, identifying both common and unique metabolites and metabolic pathways associated with MS, especially amino acid metabolic disorders, including glycine, serine, and threonine metabolism, D-glutamine and D-glutamate metabolism, which may play critical roles in regulating different metabolic dysfunctions and worth further exploration in MS pathogenesis, which might provide insights for the effective prevention and treatment of MS in various populations.

Chronic inflammation is a hallmark for Metabolic Syndrome (MetS). It is also one of the most important risk factors for insulin resistance and metabolic disorders. Inflammasomes, which are intracellular multiprotein complexes within the innate immune system, regulate the production and maturation of pro-inflammatory cytokines including interleukin-1β (IL-1β) and IL-18 upon sensing pathogens or danger signals in the cytosol. A growing body of evidence indicates that inflammasomes play a pivotal role in the pathophysiology and progression of metabolic diseases, as deficiency in the key component of inflammasomes protects mice from high fat diet induced obesity and insulin resistance. Thus, in this review, we will summarize the role of inflammasomes in MetS and how to treat MetS by targeting inflammasomes. This may provide novel insights and therapeutic targets for treating metabolic disorders.

Dyslipidemia is a major contributor to various diseases, including atherosclerotic cardiovascular disease and obesity. Treatment strategies for dyslipidemia continue to evolve as our understanding of this metabolic disorder and potential therapeutic candidates advance. Notably, fucoidan demonstrates promising effects in ameliorating dyslipidemia in rodents, although their lipid metabolism differs significantly from humans. This study, investigates the lipid-regulatory effects of Fucus vesiculosus-derived fucoidan (FvF) and elucidates the underlying mechanisms of action using New Zealand rabbits fed a high-fat diet, whose lipid profiles closely resemble those of patients with dyslipidemia. The results demonstrate that FvF intervention ameliorates dyslipidemia and lipid deposition in a dose-dependent manner. Mechanistically, FvF intervention modulates the expression levels of multiple molecules involved in lipid transport, fatty acid synthesis and beta-oxidation, and redox balance, as revealed by quantitative reverse transcription polymerase chain reaction, western blotting, and proteomic analysis. This study is the first to report that FvF, consisting of alternating [→4)-α-L-Fucp(1 → 3)-α-L-Fucp(1→] glycosyls ameliorates dyslipidemia by directly modulating lipid metabolism and indirectly attenuating oxidative stress. These findings suggest that FvF holds significant potential as a candidate for the treatment of lipid disorder-related diseases.

Cuproptosis is a new mode of cell death that is closely related to mitochondrial stress. The purpose of this study is to investigate the amount of copper, copper-associated genes DLAT and FDX1 oxidative stress (OS) status in obesity. Since there is a close relationship between OS and cuproptosis, evaluating the effect of various strategies to reduce OS, including quercetin (QUER) and caloric restriction (CR), is another goal of this study. In this study, 30 male BALB-C mice aged 8 weeks and weighing 25 g, including the groups receiving normal diet (ND), ND with QUER (15 mg/kg, IP) and CR, a high-fat diet (HFD) with the QUER, CR or a combination of both were used. The activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione reductase (GR), amount of copper in the liver and kidney tissues, and expression of DLAT and FDX1 genes were measured in all studied groups. The amount of copper in the liver and kidney tissue as well as the expression of FDX1 and DLAT in the HFD group increased significantly compared with the ND group. QUER, CR or their combination could significantly reduce the amount of copper as well as the expression of FDX1 and DLAT in liver and kidney tissues. QUER and CR, also significantly increased the activity of GR, SOD and GPX in serum, liver, and kidney tissues. Based on the results, QUER, CR and especially the simultaneous use of both, was able to reduce the amount of copper and its related cuproptosis. These effects may reduce cuproptosis-associated cell death. Therefore, the use of antioxidants and CR may be a promising solution to protect the human body against the effects of cuproptosis in conditions like obesity.

Metabolic syndrome (MetS) is characterized by central obesity, insulin resistance, hypertension, dyslipidemia, and chronic inflammation, significantly increasing the risk of cardiovascular disease and type 2 diabetes. Effective management of MetS is critical, with exercise being a key intervention. This review analyzed the effects of different exercise intensities-low, moderate, and high-intensity interval training (HIIT)-on metabolic health, oxidative stress (OS), inflammation, and cardiovascular function. A search of Medline, PEDro, and EBSCO identified 2251 articles, with 159 studies published between 1999 and 2025 included after screening. Low-intensity exercise improved insulin sensitivity, reduced OS markers (e.g., MDA, 8-OHdG), and enhanced antioxidant enzyme activity. Moderate-intensity exercise showed similar benefits with notable reductions in inflammatory markers (e.g., IL-1β, TNF-α). HIIT promoted fat loss and improved metabolic markers but temporarily increased OS and inflammation. Dietary strategies also play a critical role. The Mediterranean diet and Dietary Approaches to Stop Hypertension (DASH) diets are well established, emphasizing nutrient-dense foods like unsaturated fats and fiber to reduce inflammation and manage weight. The ketogenic diet (KD), a high-fat, low-carbohydrate approach, has recently gained attention for its metabolic benefits. KD induces ketosis, improving insulin sensitivity, reducing triglycerides, and enhancing fat oxidation. Studies show KD effectively reduces body weight and glucose levels, though long-term adherence and nutrient deficiencies remain challenges. Intermittent fasting also showed potential benefits, though effects on glucose metabolism were inconsistent. This review underscores the need for tailored approaches combining exercise, diet, and fasting to optimize MetS outcomes, offering integrative strategies for prevention and management.

Background/Objectives: Major depressive disorder (MDD) is a major global health concern that is intimately linked to neuroinflammation, oxidative stress, mitochondrial dysfunction, and complicated metabolic abnormalities. Traditional antidepressants frequently fall short, highlighting the urgent need for new, safer, and more acceptable therapeutic techniques. Phytochemicals, i.e., natural antidepressants derived from plants, are emerging as powerful plant-based therapies capable of targeting many pathogenic pathways at the same time. Summary: This narrative review synthesizes evidence from preclinical and clinical studies on the efficacy of phytochemicals such as curcumin, polyphenols, flavonoids, and alkaloids in lowering depressed symptoms. Consistent data show that these substances have neuroprotective, anti-inflammatory, and antioxidant properties, altering neuroimmune interactions, reducing oxidative damage, and improving mitochondrial resilience. Particularly, polyphenols and flavonoids have great therapeutic potential because of their capacity to penetrate the blood-brain barrier, inhibit cytokine activity, and encourage neuroplasticity mediated by brain-derived neurotrophic factor (BDNF). Despite promising results, the heterogeneity in study designs, phytochemical formulations, and patient demographics highlights the importance of thorough, standardized clinical studies. Conclusions: This review identifies phytochemicals as compelling adjuvant or independent therapies in depression treatment, providing multimodal mechanisms and enhanced tolerability. Additional research into improved dosage, pharmacokinetics, long-term safety, and integrative therapy approaches is essential. Using phytotherapeutics could considerably improve holistic and customized depression care, encouraging new research routes in integrative neuroscience and clinical psychiatry.

Hibiscus sabdariffa L. (HS) has been investigated as an alternative treatment for metabolic syndrome (MetS), as it affects all MetS components with low side effects simultaneously; however, clinical evidence regarding its efficacy compared with placebo is inconsistent. This study assessed how the aqueous calyx extract of HS influences insulin resistance and MetS parameters and examined the safety effects on liver, kidney, and hematological indexes in participants with abdominal obesity and mild MetS symptoms.

In this double-blind, randomized, placebo-controlled trial, 108 participants with MetS were randomly assigned to take 1000-mg HS (45.04 mg/day in total polyphenols) or placebo daily for 12 weeks. Insulin resistance (HOMA-IR), glycemic markers, body mass index (BMI), waist circumference (WC), lipid profiles, and blood pressure were assessed at baseline, 6 weeks, and 12 weeks. Additionally, liver and kidney function indicators along with hematological parameters were evaluated.

Compared with placebo, HS did not significantly affect HOMA-IR, glycemic markers, BMI, WC, lipid profile, or blood pressure. Although HS did not significantly alter the lipid profile overall, serum low-density lipoprotein (LDL) levels decreased significantly at 12 weeks compared with baseline (- 7.98 mg/dL, [95 % CI, - 14.80, - 1.15]). Additionally, HS did not cause significant liver or kidney function or hematological changes compared with placebo.

Taking 1000-mg HS daily for 12 weeks seems to be safe. Placebo and HS groups showed good clinical results, and the extract was not associated with improved metabolic parameters in individuals with abdominal obesity and mild MetS symptoms, with the exception of lower serum LDL.

Overactive bladder (OAB) is a syndrome marked by urinary urgency. Given the crucial role of metabolic anomalies in the pathogenesis of OAB, the aim of this study was to investigate the associations between different triglyceride glucose index (TyG)-related indicators and OAB.

9024 participants aged ≥ 20 years from NHANES 2005-2018 were involved. Weighted multivariate logistic regression was employed to assess the relationship between three TyG-related indicators and OAB with subgroup and interaction analyses. In addition, ROC, DeLong's test and confusion matrix were further utilized to assess the predictive power of different indicators for OAB in the total population versus different subgroups of the population.

TyG-related indicators were positively associated with OAB. The associations were statistically different in age and physical activity subgroups (all p for interaction < 0.1). In the whole population, TyG-WHtR demonstrated the highest predictive ability, with the largest AUC of 0.625 (95 %CI: 0.609, 0.641), and was relatively more predictive in the < 60 years and moderate-to-vigorous physical activity subgroups.

Positive associations of TyG-related indicators with OAB were observed. TyG-WHtR has the strongest predictive performance for OAB in the total population.

Reactive oxygen species (ROS), a class of highly reactive molecules, are closely linked to the pathogenesis of various cancers. While ROS primarily originate from normal cellular processes, external stimuli can also contribute to their production. Cancer cells typically exhibit elevated ROS levels due to disrupted redox homeostasis, characterized by an imbalance between antioxidant and oxidant species. ROS play a dual role in cancer biology: at moderate levels, they facilitate tumor progression by regulating oncogenes and tumor suppressor genes, inducing mutations, promoting proliferation, extracellular matrix remodeling, invasion, immune modulation, and angiogenesis. However, excessive ROS levels can cause cellular damage and initiate apoptosis, necroptosis, or ferroptosis.

This review explores molecular targets involved in redox homeostasis dysregulation and examines the impact of ROS on the tumor microenvironment (TME). Literature from recent in vitro and in vivo studies was analyzed to assess how ROS modulation contributes to cancer development and therapy.

Findings indicate that ROS influence cancer progression through various pathways and cellular mechanisms. Targeting ROS synthesis or enhancing ROS accumulation in tumor cells has shown promising anticancer effects. These therapeutic strategies exhibit significant potential to impair tumor growth while also interacting with elements of the TME.

The ROS serve as both promoters and suppressors of cancer depending on their intracellular concentration. Their complex role offers valuable opportunities for targeted cancer therapies. While challenges remain in precisely modulating ROS for therapeutic benefit, they hold promise as synergistic agents alongside conventional treatments, opening new avenues in cancer management.

Ambient air pollution is a serious public health issue worldwide. A growing number of studies has highlighted the negative effects of air pollution on metabolic syndrome (MetS) and its components, including abdominal obesity, disorders of lipid metabolism, elevated blood pressure, and impaired fasting blood glucose. This review provides a brief overview of epidemiological and genetic interaction studies of the links between chronic exposure to ambient air pollution and MetS and its components, as well as plausible mechanisms underlying these relationships. The cumulative evidence suggests that long-term exposure to air pollution, especially particulate matter, increases the risk of MetS and its components. These associations can be partly modified by baseline characteristics, lifestyle, and health conditions. Gene-by-air-pollution interaction studies, limited to candidate genes in the past, have recently been conducted at an expanded genome-wide level. However, more such studies are needed to comprehensively understand the genetics involved in the association between air pollution and MetS. Mechanistic evidence suggests potential biological pathways, including inflammation, oxidative stress, and endothelial dysfunction.

Calcific aortic valve disease (CAVD) is a progressive disease, of which the 2-year mortality is >50% for symptomatic disease. However, there are currently no pharmacotherapies to prevent the progression of CAVD unless transcatheter or surgical aortic valve replacement is performed. The prevalence of diabetes among CAVD has increased rapidly in recent decades, especially among those undergoing aortic valve replacement. Diabetes and its comorbidities, such as hypertension, hyperlipidemia, chronic kidney disease and ageing, participated jointly in the initiation and progression of CAVD, which increased the management complexity in patients with CAVD. Except from hyperglycemia, the molecular links between diabetes and CAVD included inflammation, oxidative stress and endothelial dysfunction. Traditional cardiovascular drugs like lipid-lowering agents and renin-angiotensin system blocking drugs have proven to be unsuccessful in retarding the progression of CAVD in clinical trials. In recent years, almost all kinds of glucose-lowering medications have been specifically assessed for decelerating the development of CAVD. Based on the efficacy for atherosclerotic cardiovascular disease and CAVD, this review summarized current knowledge about glucose-lowering medications as promising treatment options with the potential to retard CAVD.

Diffuse large B-cell lymphoma (DLBCL) as among the most common lymphomas is associated with insulin resistance (IR). The triglyceride-glucose (TyG) index, generally considered a surrogate marker for IR, has an uncertain prognostic value in DLBCL.

We conducted a retrospective analysis of DLBCL patients who received R-CHOP therapy at the Second Affiliated Hospital of Nanchang University from January 2011 to December 2023. Univariate and multivariate Cox regression analyses were performed to identify independent prognostic factors for overall survival (OS). Boruta algorithm was employed to strengthen the robustness of our analysis. Restricted cubic spline (RCS) analysis was used to explore the potential nonlinear relationship between the TyG index and OS. Subgroup analyses were conducted to assess the prognostic value of the TyG index across different patient subgroups. Finally, a nomogram model based on the TyG index was developed, and its predictive performance was evaluated using the area under the receiver operating characteristic curve (AUROC), calibration curves, and decision curve analysis (DCA).

A total of 186 DLBCL patients were included in this study. Univariate and multivariate Cox regression analyses identified the TyG index, Age, ECOG performance status, Ann Arbor stage, and lactate dehydrogenase levels as independent prognostic factors for DLBCL. The Boruta algorithm confirmed these variables as the most important prognostic factors. Kaplan-Meier analysis revealed significantly poorer OS in the high TyG index group. RCS analysis demonstrated a non-linear relationship between the TyG index and OS. Subgroup analyses further validated the TyG index as a significant prognostic factor across various patient subgroups. The TyG-based nomogram model outperformed the conventional International Prognostic Index (IPI), with AUROCs of 0.878, 0.809, and 0.867 for 1-year, 3-year, and 5-year OS, respectively. Calibration curves showed good agreement between the nomogram predictions and actual outcomes, and DCA highlighted the high clinical utility of the model.

The TyG index is an independent prognostic factor in DLBCL patients, and the TyG-based nomogram model provides enhanced predictive accuracy compared to the IPI. Its simplicity and low cost make it a valuable tool for routine clinical prognostic assessment in DLBCL patients.

Carbohydrate metabolism disorders (CMDs), including prediabetes and type 2 diabetes mellitus (T2DM), are increasingly prevalent in the aging population. Oxidative stress (OxS) plays a pivotal role in CMD pathogenesis, with extracellular superoxide dismutase (SOD3) and catalase (CAT) serving as critical antioxidant defenses. Additionally, microRNAs (miR-21 and miR-30b) regulate the oxidative and inflammatory pathways, yet their roles in elderly CMD patients remain unclear. This study evaluated miR-21 and miR-30b expression alongside SOD3 and CAT plasma levels in individuals aged ≥ 65 years (n = 126) categorized into control (n = 38), prediabetes (n = 37), and T2DM (n = 51) groups. Quantitative PCR assessed miRNA expression, while ELISA measured the enzyme levels. SOD3 levels were significantly reduced in CMDs, particularly in T2DM, whereas miR-21 was upregulated. A negative correlation between SOD3 and miR-21 was strongest in T2DM, suggesting a regulatory interplay. Neither CAT levels nor miR-30b expression differed among groups. Logistic regression indicated SOD3 as a protective biomarker, with each 1 ng/mL increase reducing the CMD risk by ~5-6%. The ROC analysis supported SOD3's diagnostic potential, while miR-21 showed a modest association. These findings highlight SOD3 downregulation and miR-21 upregulation as potential contributors to CMD progression in elderly patients, warranting further research into their mechanistic roles and therapeutic potential.

Due to an aging population and the prevalence of illnesses associated with modern lifestyles, mushrooms, well known for their nutritional value and health-promoting properties, are becoming an increasingly important part of the diet. They are consumed in various forms, including food, nutraceuticals, and dietary supplements. A relatively new trend involves incorporating mushrooms or their components as additives and supplements to enhance the quality and functionality of traditional food products. The processing and preservation methods of fresh mushrooms can significantly impact the activity of resulting powders, extracts, or other functional forms used in food additives, supplements, and fortified foods. The functional benefits of mushrooms are frequently attributed to their antioxidant and anti-inflammatory properties. However, to date, the literature lacks comprehensive reviews that consolidate existing knowledge on mushroom-based food additives and products enriched with them. Therefore, this review aims to compile and methodically analyze the existing data in this field, identify existing knowledge gaps, and outline future perspectives for the development and application of such products. Special attention is given to food supplementation with microencapsulated additives, which represent a promising form of functional powders. All these aspects are evaluated in terms of their antioxidant and anti-inflammatory properties. Finally, future perspectives on improving the health benefits of food through mushroom-based additives are discussed.

Diabetic cardiomyopathy (DCM) is a common and fatal cardiac complication caused by diabetes, with its pathogenesis involving various forms of cell death and mitochondrial dysfunction, particularly ferroptosis and mitochondrial injury. Recent studies have indicated that ferroptosis and mitochondrial damage play crucial roles in the onset and progression of DCM, though their precise regulatory mechanisms remain unclear. Of particular interest is the interaction between ferroptosis and mitochondrial damage, as well as their synergistic effects, which are not fully understood. This review summarizes the roles of ferroptosis and mitochondrial injury in the progression of DCM and explores the molecular mechanisms involved, with an emphasis on the interplay between these two processes. Additionally, the article offers an overview of targeted drugs shown to be effective in cellular experiments, animal models, and clinical trials, analyzing their mechanisms of action and potential side effects. The goal is to provide insights for future drug development and clinical applications. Moreover, the review explores the challenges and prospects of multi-target combination therapies and personalized medicine interventions in clinical practice to offer strategic guidance for the comprehensive prevention and management of DCM.

The cultivation and processing of fruits generate a wide range of by-products (e.g., pulp, seeds, pomace, leaves, and stems), which are often underutilized despite being rich sources of phenolic compounds with well-documented bioactive properties. The bioactive potential of these compounds has attracted significant interest from both the pharmaceutical and food sectors, offering opportunities for their use in functional foods, dietary supplements, natural medicines, and additives. Among these, phenolic acids have shown promising potential in modulating risk factors associated with metabolic syndrome (MetS), a condition encompassing hypertension, dyslipidemia, hyperglycemia, and abdominal obesity, and contributing significantly to cardiovascular disease. Given the global burden of MetS and the need for novel preventive strategies, numerous studies have investigated the bioactivity of phenolic acids derived from fruit by-products. In this review, we critically examine recent studies regarding the phenolic acid composition of fruit-derived by-products and their biological activity in relation to MetS-related risk factors. This work aims to synthesize current findings, highlight prevailing research trends, and identify existing gaps in the literature to inform future research and promote the sustainable use of fruit by-products in the prevention and management of MetS.

A high-fat diet is a key factor contributing to hyperlipidemia. Perilla seed oil, a plant-based source of omega-3, has the potential to reduce this risk. However, its effects have not been fully established. This study aimed to evaluate the effects of perilla seed oil on blood lipid levels, oxidative stress, and inflammation in rats induced with hyperlipidemia through a high-fat diet. Male Wistar rats were administered perilla seed oil at a dosage of 0.67 g/kg body weight per day for 8 weeks. The results showed that perilla seed oil significantly reduced triglyceride levels by 38.00% and 41.88% and total cholesterol levels by 17.16% and 15.91% in the high-fat diet and normal diet groups, respectively (p < 0.05). However, perilla seed oil had no significant effect on HDL and LDL levels. Additionally, perilla seed oil supplementation significantly reduced malondialdehyde (MDA) levels, a biomarker of oxidative stress, by 68.18% in the high-fat diet group and 29.72% in the normal diet group. Regarding its anti-inflammatory effects, perilla seed oil reduced interleukin-6 (IL-6) levels by 15.21% and 64.27% in the high-fat diet and normal diet groups, respectively (p < 0.05). These findings suggest that perilla seed oil has the potential to reduce the risk of metabolic syndrome.

Perfluorohexane sulfonate (PFHxS) is a persistent environmental contaminant linked with several health implications. Humans are exposed to PFHxS mainly through ingestion. Studies have reported that a diet deficient in essential nutrients may have confounding effect on the toxicity outcome of chemicals. We evaluated the potential impact of PFHxS exposure on the reproductive damage in animals maintained on the diet deficient in protein. Female Wistar rats (n = 6) were divided as controls and treatment groups (5 ppm and 25 ppm PFHxS, protein deficient, protein deficient +5 ppm PFHxS and protein deficient +25 ppm PFHxS). PFHxS exposure disrupted the estrous cycle with an increased duration of the diestrus stage at 25 ppm and protein deficient + 25 ppm PFHxS showing 55.56 % and 78.77 % disorder, respectively. There was a significant elevation (P < 0.01) in LH/FSH ratio and reduction in testosterone (P < 0.01), estradiol (P < 0.01), and progesterone (P < 0.001) in protein deficient + 25 ppm PFHxS group. A high order of increase in lipid profile parameters was found in protein deficient + 25 ppm PFHxS group. However, high-density lipoprotein decreased in this group. Protein deficient + 25 ppm PFHxS group animals also revealed high level of oxidative stress. Histopathological findings revealed the presence of cystic follicles and theca cell degeneration in ovaries in the protein deficient + 25 ppm PFHxS group with a significant decrease (P < 0.01) in the myometrium and endometrial area of uterus. The combined effect of protein deficiency and PFHxS exposure caused a greater reprotoxicity compared to either factor alone implying an increased vulnerability of reproductive function in malnourished populations to environmental contaminants.

Hyperlipidemia, marked by high levels of fats in the blood, is a major risk factor for non-communicable diseases such as type 2 diabetes, cardiovascular diseases, and cancer. It has been linked to the action of reactive oxygen species and the formation of advanced glycation end products. Current treatments for hyperlipidemia, like orlistat, simvastatin, and atorvastatin, often present undesirable side effects, prompting the need for new therapeutic agents that are safer, more effective, cost-efficient, and have fewer side effects. In this context, new compounds, specifically propano- and butanosulfonic acids with 9-substituted quinobenzothiazinyl substituents, were synthesized through reactions with 9-substituted quinobenzothiazines and propane sultone or butane sultone. These novel quinobenzothiazine derivatives were verified using 1H NMR, 13C NMR, and HR-MS techniques. The research focused on assessing these compounds for their toxicity, ability to prevent glycation, antioxidant properties, and their potential to combat hyperlipidemia. Toxicity was evaluated on the 3T3 L1 fibroblast cell line using the MTT assay. The capacity to prevent glycation was tested with bovine serum albumin-methylglyoxal and bovine serum albumin-glucose systems. This study measured total reactive oxygen species in the 3T3 L1 cell line using 2',7'-dichlorodihydrofluorescein diacetate staining, and antioxidant capacity was assessed through DPPH scavenging and metal ion chelation tests. The effectiveness against hyperlipidemia was determined by targeting cholesterol esterase and pancreatic lipase activities, with concentrations of the compounds 5 to 12 ranging from 0.0245 to 0.268 μM. Standard drugs such as orlistat, simvastatin, statins, and aminoguanidine were used as positive controls in various assays. Additionally, computational docking studies with AutoDock Vina were performed. The resulting findings indicated that the compounds were non-toxic to cells, effectively inhibited key enzymes related to hyperlipidemia, and showed significant antioxidant properties, including the prevention of advanced glycation end-product formation. Compounds 11 and 12 demonstrated the highest activity levels. These promising results highlight the potential of new quinobenzothiazine derivatives as lead compounds for the development of antihyperlipidemic drugs, although further research is necessary to confirm their efficacy and safety.

Diabetes mellitus (DM) is a chronic endocrine and metabolic disorder characterized by persistent hyperglycemia that poses serious threats to human health and quality of life. The morbidity, disability, and mortality rates of cardiovascular complications stemming from chronic hyperglycemia are primary factors affecting the lifespan of patients with diabetes. Currently, there is no cure for DM. Standard biomedical treatments mostly control the symptoms using insulin injections or oral hypoglycemic drugs. Although the effect of standard biomedical therapy is remarkable, its long-term use is prone to toxic side effects. Numerous studies have recently found that Traditional Chinese Medicine (TCM) has strong advantages in the prevention and treatment of DM and cardiovascular complications (DACC). The collection, processing, preparation and clinical use of TCM are guided by the theory of TCM and follow the "holistic concept." Multiple components, pathways, and targets form the basis for the use of TCM in treating multiple parts and organs of the body simultaneously. TCM is mainly derived from natural medicines and their processed products and has fewer side effects. TCM is clinically used as compound prescriptions, botanical drugs, and monomers. TCM, either independently or in combination with standard biomedical treatments, has shown unique therapeutic advantages. This review aimed to explore the recently reported mechanisms of action of TCM in the prevention and treatment of DACC. These findings will aid the optimization of the current therapy or formation of a therapeutic schedule for integrated TCM and standard biomedical treatments.

Chronic obstructive pulmonary disease (COPD) is a progressive and debilitating condition characterized by airflow limitations and systemic inflammation. The interaction between the metabolic and inflammatory pathways plays a key role in disease progression, with leptin and insulin emerging as pivotal metabolic regulators. Leptin, an adipokine that regulates energy homeostasis, and insulin, the primary regulator of glucose metabolism, are both altered in COPD patients. This narrative review provides an in-depth examination of the roles of leptin and insulin in COPD pathogenesis, focusing on the molecular mechanisms through which these metabolic regulators interact with inflammatory pathways and how their dysregulation contributes to a spectrum of extrapulmonary manifestations. These disturbances not only exacerbate COPD symptoms but also increase the risk of comorbidities such as metabolic syndrome, diabetes, cardiovascular disease, or muscle wasting. By exploring the underlying mechanisms of leptin and insulin dysregulation in COPD, this review underscores the significance of the metabolic-inflammatory axis, suggesting that restoring metabolic balance through leptin and insulin modulation could offer novel therapeutic strategies for improving clinical outcomes.

Chronic inflammation is an important component of many diseases, including autoimmune diseases, intracellular infections, dysbiosis and degenerative diseases. An important element of this state is the mainly positive feedback between inflammatory cytokines, reactive oxygen species (ROS), nitric oxide (NO), increased intracellular calcium, hypoxia-inducible factor 1-alpha (HIF-1α) stabilisation and mitochondrial oxidative stress, which, under normal conditions, enhance the response against pathogens. Autophagy and the nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant response are mainly negatively coupled with the above-mentioned elements to maintain the defence response at a level appropriate to the severity of the infection. The current review is the first attempt to build a multidimensional model of cellular self-regulation of chronic inflammation. It describes the feedbacks involved in the inflammatory response and explains the possible pathways by which inflammation becomes chronic. The multiplicity of positive feedbacks suggests that symptomatic treatment of chronic inflammation should focus on inhibiting multiple positive feedbacks to effectively suppress all dysregulated elements including inflammation, oxidative stress, calcium stress, mito-stress and other metabolic disturbances.

Tamarillo (Solanum betaceum Cav.) is rich in polyphenols, anthocyanins, and carotenoids, making it a promising candidate for functional food development. This study investigated phytochemical profiles and bioactivities in different tamarillo parts. Various parts of tamarillo were extracted using water and ethanol (0-95%), with 95% ethanol yielding the highest content of bioactive compounds in the peel, pulp, mucilage, and whole fruit, while 75% ethanol was more effective for the seeds. Among tamarillo components, the peel exhibited the highest concentrations of hydroxycinnamoyl derivatives, anthocyanins, and carotenoids, along with superior antioxidant capacity, including strong scavenging activity against 2,2-diphenyl-1-picrylhydrazyl (DPPH) radicals (EC50, 45.26 µg extract/mL) and high reducing power (EC50, 113.3 µg extract/mL). The peel extract exhibited the strongest inhibitory effects on α-glucosidase (IC50, 1.623 mg/mL) and angiotensin-converting enzymes (IC50, 1.435 mg/mL). In contrast, the pulp extract demonstrated the highest inhibitory activity against pancreatic lipase (IC50, 0.882 mg/mL) and α-amylase (IC50, 2.369 mg/mL). These findings suggest that tamarillo extracts possess potent antioxidant activity and enzyme-inhibitory properties related to metabolic syndrome (MetS). However, gastrointestinal digestion simulation influenced the bioactive compound content and bioactivities. Overall, tamarillo has promising potential as a functional ingredient for MetS prevention, but processing strategies are needed to retain its bioactive properties.

Background/Objectives: Inflammatory sarcopenia, characterized by muscle weakness exacerbated by chronic systemic inflammation, has emerged as a critical factor in fall risk among older adults. While previous studies have examined sarcopenia and inflammation independently, few have investigated their combined impact on mobility impairments and fall susceptibility, particularly in immunocompromised individuals. This study aimed to assess the role of inflammatory sarcopenia in increasing fall risk by comparing functional performance, muscle strength, and inflammatory biomarkers across three groups: healthy older adults, individuals with non-inflammatory sarcopenia, and those with inflammatory sarcopenia. A secondary objective was to evaluate fall incidence in immunocompromised versus non-immunocompromised individuals. Methods: A prospective observational study was conducted on 250 adults aged ≥65 years, categorized based on inflammatory status and muscle health. Functional assessments included handgrip strength, the Timed Up and Go (TUG) test, and fall frequency analysis. Inflammatory status was determined by measuring C-reactive protein (CRP) and interleukin-6 (IL-6) levels. Multivariate regression models were used to identify predictors of fall risk. Results: Participants with inflammatory sarcopenia exhibited significantly higher CRP and IL-6 levels, greater muscle weakness, poorer mobility performance, and a fourfold increase in fall incidence compared to controls (p < 0.001). Immunocompromised individuals had nearly double the fall risk of their non-immunocompromised counterparts (p < 0.001). TUG test performance was the strongest fall predictor. Conclusions: Our findings highlight the importance of integrating fall prevention strategies that not only focus on muscle-strengthening programs but also include regular screening for inflammatory markers. Given the strong association between systemic inflammation, muscle weakness, and fall risk, identifying and managing chronic inflammation may play a crucial role in reducing mobility impairments and improving outcomes in older adults.

Conventional post-stroke edema management strategies are limitedly successful as in multiple cases of hemorrhagic transformation is being reported. Clinically, acute-ischemic-stroke (AIS) intervention by endovascular mesenchymal stem cells (MSCs) have shown benefits by altering various signaling pathways. Our previous studies have reported that intra-arterial administration of 1*105 MSCs (IA-MSCs) were beneficial in alleviating post-stroke edema by modulating PKCδ/MMP9/AQP4 axis and helpful in preserving the integrity of blood-brain-barrier (BBB). However, the role of mitochondrial dysfunction and ROS generation post-AIS cannot be overlooked in context to the alteration of the BBB integrity and edema formation through the activation of inflammatory pathways. The anti-inflammatory activity of IA-MSCs in stroke has been reported to be regulated by sirtuin-1 (SIRT-1). Hence, the relationship between SIRT-1 and AQP4 towards regulation of post-stroke edema needs to be further explored. Therefore, the present study deciphers the molecular events towards AQP4 upregulation, mitochondrial dysfunction and BBB disruption in context to the modulation of SIRT-1/PKCδ/NFκB loop by IA-MSCs administration.

Ovariectomized SD rats were subjected to focal ischemia. SIRT-1 activator, SIRT-1 inhibitor, NFkB inhibitor and IA-MSCs were administered at optimized dose. At 24 h of reperfusion, behavioral tests were performed, and brains were harvested following euthanasia for molecular studies.

IA-MSCs downregulated AQP4, PKCδ and NFkB expression, and upregulated SIRT-1 expression. SIRT-1 upregulation renders mitochondrial protection via reduction of oxidative stress resulting in BBB protection.

IA-MSCs can modulate SIRT-1 mediated AQP4 expression via mitochondrial ROS reduction and modification of NFkB transcriptional regulation.

Emerging evidence suggests that in-utero exposure to microplastics (MPs) may have physiological consequences for fetal development, yet human data remain limited. This study investigates the association between placental microplastic exposure and umbilical liver enzyme levels as markers of fetal hepatic function. A prospective cohort study was conducted in Shenyang, China, including 1057 pregnant women. Placental microplastic quantification was performed using LD-IR chemical imaging, targeting polyvinyl chloride (PVC), polypropylene (PP), and polybutylene succinate (PBS). Umbilical cord blood was collected at delivery, and liver enzyme levels alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) were analyzed using biochemical assays. Associations were assessed via multivariable regression models adjusting for maternal and socioeconomic confounders. Mixture effects were examined using Bayesian Kernel Machine Regression (BKMR) and quantile g-computation (g-comp). Placental microplastics were detected in most samples (PVC: 88.4 %, PP: 88.8 %, PBS: 89.1 %), with a median total MPs of 12 particles per 10 g of tissue (IQR: 8). Higher placental PVC particles was significantly associated with increased ALP levels (β = 28.07, 95 % CI: 6.65-49.49, p = 0.01). PP exposure correlated positively with ALT (β = 0.63, 95 % CI: 0.01-1.25, p = 0.05) and AST (β = 3.42, 95 % CI: 0.87-5.96, p = 0.01). Both PP and total MPs burden exhibited strong associations with GGT elevation (p < 0.01). Mixture analysis revealed significant overall effects on ALP (β = 30.04, 95 % CI: 11.15-48.92, p < 0.01), AST (β = 7.30, 95 % CI: 4.33-10.27, p < 0.01), and GGT (β = 22.98, 95 % CI: 7.49-38.46, p < 0.01), with ALT showing a suggestive positive trend. Our findings provide novel evidence that placental MP exposure is associated with altered fetal liver enzyme levels, particularly ALP, AST, and GGT, indicating potential impacts on hepatic function. These results underscore the need for further investigation into the underlying mechanisms and long-term health implications of prenatal MP exposure.

Despite certain studies indicating hearing impairments in individuals with polycystic ovary syndrome (PCOS), the correlation between PCOS and sensorineural hearing loss (SNHL) remains inconclusive. This study aimed to investigate the association between PCOS and SNHL.

A systematic literature search was conducted using PubMed, MEDLINE, EMBASE, and the Cochrane Library from inception to June 24, 2024.

This meta-analysis included cross-sectional, case-control, or cohort studies examining the association between PCOS and SNHL without language or regional restrictions. Case reports, case series, animal studies, and in vitro studies were excluded. We adhered to Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines and utilized the Newcastle-Ottawa Scale to assess the risk of bias in the included studies.

After performing the systematic review, we conducted a meta-analysis that included 489 patients from 5 studies: 349 patients with PCOS and 140 age- and sex-matched controls without PCOS. The meta-analysis compared the mean differences in frequency-specific pure-tone thresholds between patients with PCOS and matched controls, providing 95% confidence intervals for these differences. Given the expected clinical heterogeneity, we employed the DerSimonian and Laird random-effects model. Our results revealed significant hearing loss at specific frequencies (1000, 4000, 8000, 10,000, 12,000, 14,000, 16,000, 18,000, and 20,000 Hz) in the PCOS group compared to the control group (P < .05). Furthermore, the degree of hearing loss is greater at higher frequencies.

This meta-analysis demonstrated an association between PCOS and SNHL, particularly at higher frequencies.

To examine Hedan tablet (HDT, )'s potential mechanisms in hyperlipidemic rats induced by a high-fat diet (HFD), as well as its regulatory effects and primary active constituents.

By using ultra-performance liquid chromatography (UPLC)-quadrupole-time-of-flight (QTOF)-tandem mass spectrometry (MS/MS), the components of HDT that can enter the circulatory system were found, aiming to investigate its active constituents with pharmacological effects. Based on network pharmacology approaches, the relevant HDT targets in the therapy of hyperlipidemia were anticipated. The possible mechanism of HDT for hyperlipidemia treatment was verified by in-vivo experiments, and the main active components of HDT for hyperlipidemia treatment were analyzed via in-vitro experiments.

UPLC-QTOF-MS/MS identified 30 components of HDT entering the circulatory system, primarily consisting of flavonoids, diterpenoids and alkaloids. The results of a network pharmacology study revealed that 30 active components mostly target 74 genes associated with hyperlipidemia. The primary active ingredients may include quercetin, kaempferol, and epicatechin, and the main gene targets may be tumor necrosis factor (TNF), interleukin-6 (IL-6), interleukin 1 beta (IL-1β), etc. The results of animal experiments demonstrated that HDT can significantly regulate the blood lipid level in rats with HFD, improve the degree of inflammatory infiltration in rat liver cells, lower TNF-α, C-reactive protein (CRP), IL-6, matrix metalloproteinase 9 (MMP9) and malondialdehyde (MDA) levels while raising total superoxide dismutase (T-SOD) level. Meanwhile, HDT can considerably lower the expression of sterol regulatory element-binding transcription factor 2 (SREBF2), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), and MMP9 while significantly increasing the expression of peroxisome proliferator-activated receptor alpha (PPAR-α) and PPAR-γ. In vitro study confirmed that quercetin and kaempferol could reduce the levels of IL-6, IL1B, MMP9 and HMGCR in the high-fat model of hepatoma G2 cells.

The mechanism by which HDT treats hyperlipidemia involves modification of the lipid metabolism targets such as downregulating SREBF2, HMGCR and MMP9, and upregulating PPAR-α and PPAR-γ, as well as anti-inflammatory and antioxidant actions. This study provides a pharmacological and biological rationale for the use of HDT in clinical hyperlipidemia management.

Hypertension, a major global health concern, is closely associated with obesity and lipid abnormalities. Remnant cholesterol (RC), a triglyceride-rich lipoprotein component, has been linked to cardiovascular diseases, but its joint impact with body mass index (BMI) on hypertension risk remains unclear.

We analyzed data from 3805 participants (mean age: 57 years; 44.3% male) in the China Health and Retirement Longitudinal Study (CHARLS) from 2011-2020. Inclusion criteria were adults aged over 45 years with complete data on blood lipids and BMI. Participants with baseline hypertension or missing covariate data were excluded. Cox proportional hazard models assessed associations, while mediation analysis explored RC's role in BMI-hypertension linkage.

Over a 9-year follow-up, 590 participants developed hypertension. Obesity (BMI ≥28.0 kg/m²) and high RC levels were independently associated with hypertension (HR: 2.18; 95% CI: 1.48-3.21 for the highest RC tertile). RC mediated 7.07% of BMI's effect on hypertension, and BMI mediated 29.3% of RC's effect.

This study highlights the intertwined roles of BMI and RC in hypertension development. Targeting both risk factors may enhance prevention strategies.

Poor prognosis of maintenance hemodialysis (MHD) patients, including cardiovascular disease (CVD) and protein-energy wasting (PEW), is strongly associated with insulin resistance (IR). Previous studies have revealed that limb ischemic preconditioning (LIPC), as an intervention, is effective in reducing inflammation and oxidative stress levels in patients. The aim of this study was to elucidate the effects of LIPC on IR indirect indices, inflammation and oxidative stress indices, and to further explore the potential mechanisms of LIPC in reducing IR indices.

A retrospective analysis was performed on 62 patients with MHD who had previously undergone limb ischemia preconditioning (LIPC) or sham surgery (Sham). General clinical and laboratory data were collected. Furthermore, to assess the IR status of MHD patients, the following indices were employed: triglyceride-glucose index (TyG), triglyceride-glucose body mass index (TyG-BMI), triglyceride-to-high-density lipoprotein cholesterol ratio (TG/HDL-C), and metabolic score of insulin resistance (METS-IR). Inflammation and oxidative stress indicators included high-sensitivity C-reactive protein (hs-CRP), hs-CRP /albumin ratio (CAR), serum malondialdehyde (MDA) and superoxide dismutase (SOD). Mediation analysis was conducted using Model 4 in the SPSS PROCESS macro version 4.1.

Following a four-week experiment, hs-CRP (15.46 ± 3.60 vs. 10.53 ± 5.42, p < 0.001), CAR (0.39 ± 0.10 vs. 0.26 ± 0.13, p < 0.001) and MDA (8.46(6.71,9.85) vs. 5.99(5.11,7.89), p = 0.001) indices were significantly decreased in the MHD patients of the LIPC group, whereas SOD indices (215.07(180.27,286.45) vs. 267.76(228.32,319.54), p = 0.012) were significantly higher. Only hs-CRP (-4.93 ± 5.68 vs. 0.16 ± 5.39, p = 0.001) and CAR (-0.14 ± 0.14 vs. -0.001 ± 0.15, p = 0.001) were significantly different in the LIPC group compared to the Sham group. In contrast, the changes in MDA (p = 0.058) and SOD (p = 0.107) were not statistically significant between groups. The intra- and inter-group differences in the four indirect indices of IR were significant (p < 0.05). The heatmap revealed a notable correlation between the changes in hs-CRP and CAR levels and the changes in the IR indirect indices. In addition, The mediation model showed that the inflammatory indicators hs-CRP played a partial mediating role in the improvement of IR indices (TyG-BMI) by LIPC.

LIPC has an excellent ability to inhibit inflammation and peroxidation. In addition, in MHD patients, inflammation plays a significant role in the process of LIPC improving IR index.