This research proposes to systematically investigate the cardioprotective mechanisms of Pericarpium Trichosanthis injection (PTI) against acute myocardial ischemia through an integrated approach combining ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) constituent profiling, UNIFI database-assisted component identification, network pharmacology-guided target prediction, molecular docking verification, and in vivo experimental validation. The multimodal methodology is designed to comprehensively uncover the therapeutic benefits and molecular pathways underlying this traditional Chinese medicine formulation.

UPLC-Q-TOF/MS and the UNIFI database were used in conjunction with a literature review to screen and validate the absorbed components of PTI. Using network pharmacology, we constructed protein-protein interaction (PPI) networks for pinpointing prospective therapeutic targets. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to identify potential signaling pathways. In vivo experiments were conducted to investigate the mechanisms by which PTI ameliorated isoproterenol-induced myocardial injury in rats. All animal experiments have adhered to ARRIVE guidelines.

UPLC-Q-TOF/MS revealed 11 core active components in PTI. Network pharmacology prioritization identified pseudoaspidin, ciryneol C, cynanoside M, daurinol, and n-butyl-β-D-fructopyranoside as central bioactive constituents within the compound-target interaction network. Topological analysis of the protein interactome highlighted AKT1, EGFR, MMP9, SRC, PTGS2, STAT3, BCL2, CASP3, and MAPK3 as the most interconnected nodes with the highest betweenness centrality. Pathway enrichment analysis established the PI3K/Akt signaling cascade as the principal mechanistic route for PTI's cardioprotective effects. Molecular docking simulations demonstrated high-affinity interactions between characteristic components (e.g., cynanoside M, darutigenol) and pivotal targets including PTGS2, MAPK3, CASP3, and BCL2. In vivo investigations showed PTI treatment markedly attenuated myocardial tissue degeneration and collagen deposition (p < 0.05), normalized electrocardiographic ST-segment deviations, and suppressed pro-inflammatory cytokine production (IL-6, TNF-α). The formulation concurrently reduced circulating levels of cardiac injury indicators (LDH, cTnI) and oxidative stress parameters (ROS, MDA), Regarding apoptosis regulation, PTI reduced Bax, caspase-3, and caspase-9, while elevating Bcl-2 (p < 0.05), effectively inhibiting myocardial cell apoptosis with all therapeutic outcomes reaching statistical significance. These findings highlight PTI's protective effects against myocardial injury through multi-target modulation of inflammation, oxidation, and apoptosis.

PTI exerts its therapeutic effects in treating acute myocardial ischemia by regulating and suppressing inflammatory responses, and inhibiting cardiomyocyte apoptosis.

This study, designed as a retrospective study, aims to investigate the clinical efficacy of Longgu Muli Decoction plus additions in treating chronic atrophic gastritis (CAG) and the changes in traditional Chinese medicine (TCM) syndromes. Sixty patients with CAG were enrolled and divided into the observation group and control group according to different treatment methods, with 30 patients in each group. The observation group received Longgu Muli Decoction plus additions, while the control group received conventional treatment. The treatment duration was 4 weeks. Clinical efficacy, TCM syndrome scores, gastrointestinal hormone levels, serum inflammatory factor levels, and sleep quality of the 2 groups were evaluated before and after treatment. Data were analyzed using SPSS 22.0 statistical software. The total effective rate in the observation group was 96.67%, significantly higher than 86.67% in the control group (P < .05). After treatment, the TCM syndrome scores, gastrointestinal hormone levels (endothelin [ET], calcitonin gene-related peptide [CGRP], epidermal growth factor [EGF]), and serum inflammatory factor levels (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], C-reactive protein [CRP]) in the observation group were significantly better than those in the control group (P < .05). Moreover, the Pittsburgh Sleep Quality Index (PSQI) total score and various subscale scores in the observation group were significantly lower than those in the control group (P < .05). Longgu Muli Decoction plus additions has significant clinical efficacy in treating CAG. It can effectively improve gastrointestinal function, reduce inflammatory reactions, and enhance sleep quality, thus demonstrating high clinical application value.

Chronic atrophic gastritis (CAG) is a critical initial step in gastric cancer tumorigenesis accompanied by high malignancy. Erianin has been proposed as a promising agent in treating precancerous lesions of gastric cancer. Considering that little work has been implemented concerning the specific role and possible regulatory mechanism of Erianin in CAG, the goal of the study is to disclose the effects and mechanism of erianin on the malignant transformation in the process of CAG. CAG cell model was generated in human gastric epithelium GES-1 cells induced by Nmethyl-N'-nitro-N-nitrosoguanidine (MNNG). CCK-8 method determined cell viability. ELISA and corresponding assay kits severally appraised the contents of inflammatory cytokines and oxidative stress markers. Cellular reactive oxygen species (ROS) formation was measured by flow cytometry analysis using DCFH-DA probe. GFP-LC3 immunofluorescence staining and Western blotting evaluated autophagy. Also, Western blotting analyzed the expression of components in mitogen activated protein kinase (MAPK)/mechanistic target of rapamycin (mTOR) signaling. The results manifested that MNNG treatment diminished the viability and autophagy whereas intensified the inflammation and oxidative stress in GES-1 cells, which were all reversed by Erianin. Besides, Erianin blocked mTOR/MAPK signaling in MNNG-exposed GES-1 cells. Autophagy inhibitor 3-methyladenine (3-MA) or p38 MAPK agonist asiatic acid partially counteracted the protection elicited by Erianin against viability loss, inflammatory reaction as well as oxidative stress in MNNG-induced GES-1 cells. Combined with the findings, Erianin might mediate autophagy to improve MNNG-elicited CAG via MAPK/mTOR signaling.

Zuojin formula (ZJF) is a well-known herbal medicine in Pharmacopoeia of China, which is widely used for gastritis. Modified Zuojin formula (MZJF) was adapted based on traditional Chinese medicine (TCM) theories concerning gastric atrophy and dysplasia, along with extensive clinical experience, has been clinically employed to treat chronic atrophic gastritis (CAG). However, the underlying mechanisms by which MZJF intervenes in CAG remain to be fully elucidated.

The aim of this study was to evaluate the effects of MZJF intervention in CAG and explore its potential mechanisms.

Four induction factors were used to establish a CAG rat model. HE and AB-PAS staining was utilized to assess the effects of MZJF in the intervention of CAG. The stomach weight index and gastric acid pH was used to assess the overall state of stomach. ELISA was used to assess the gastric mucosal inflammatory response. Using transmission electron microscopy to observe chief cells and parietal cells, we evaluated the improvement of ultrastructure by MZJF. Through network pharmacology analysis, the possible regulatory mechanism of MZJF in CAG was preliminarily explored. Binding interactions between MZJF components and predicted targets were explored using molecular docking. Subsequently, quantitative real-time PCR (qRT-PCR), Western blot, biochemical analysis and TUNEL staining were applied to validate the effect of MZJF on predicted pathway.

MZJF treatment ameliorated gastric mucosal pathology, inflammation, cellular ultrastructural damage and PG levels, halted the exacerbation of CAG in rats, along with a reduction in stomach weight index and gastric acid pH. A total of 79 compounds in MZJF targeting 203 CAG-related molecules were identified through network pharmacology. Enrichment analysis of the core targets was focused on the hypoxia inducible factor-1α (HIF-1α) signaling pathway. Molecular docking results identified HIF-1α as stable binding targets for MZJF primary components. Subsequently, PCR, WB, and biochemical results showed that MZJF suppressed the gene and protein expression levels of HIF-1α and its downstream molecules including glycolytic enzymes and transporters, modulated glucose, pyruvic acid and lactate levels in gastric mucosal tissue. Moreover, MZJF induced apoptosis of gastric epithelial cells, as evidenced by the upregulation of cleaved caspase-3, Bax, Bax/Bcl-2 and TUNEL positive cells ratio.

MZJF suppressed the HIF-1α-mediated glycolytic pathway, and promoted cell apoptosis, thereby halting the malignant transformation of CAG. The study provides a valuable reference point for applying TCM in preventing and treating CAG.

Characterized by inflammation of the gastric mucosa, atrophy of gastric gland cells, and intestinal metaplasia, Chronic Atrophic Gastritis (CAG) is a precancerous lesion disease. In traditional Chinese medicine, Rhizoma Coptidis (RC) is extensively used for treating gastrointestinal disorders, mainly because RC alkaloids-based extracts are the main active pharmaceutical ingredients. Total Rhizoma Coptidis extracts (TRCE) is a mixture of Rhizoma Coptidis extracts from Rhizoma Coptidis with alkaloids as the main components. However, the efficacy and mechanism of TRCE on CAG need further study.

To explore the therapeutic effect and underlying mechanisms of action of TRCE on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced chronic atrophic gastritis (CAG) using network pharmacological analysis.

The amelioration effect of TRCE on CAG was evaluated in MNNG-induced CAG mice. The pathological severity of the mice was evaluated through H&E staining. Detection of gastric mucosal parietal cell loss was conducted using immunofluorescence staining, and serum indices were measured using ELISA. Additionally, the active compounds and drug targets of Rhizoma Coptidis were curated from the STP, SEA, and TCMSP databases, alongside disease targets of CAG sourced from PharmGkb, OMIM, and GeneCards databases. By mapping drug targets to disease targets, overlapping targets were identified. A shared protein-protein interaction (PPI) and drug target network were constructed for the overlapping targets and analyzed for KEGG enrichment.

The results of animal experiments demonstrate that TRCE has the potential to improve the CAG process in mice. In conjunction with disease characteristics, cyberpharmacology analysis has identified nine core compounds, 151 targets, 10 core targets, and five significant inflammatory pathways within the compound-target-pathway network. Furthermore, there is a remarkable coincidence rate of 98% between the core compound targets of TRCE and the targets present in the CAG disease database. The accurate search and calculation of literature reports indicate that the coverage rate for 121 predicted core targets related to CAG reaches 81%. The primary characteristic of CAG lies in its inflammatory process. Both predicted and experimental findings confirm that TRCE can regulate ten key inflammation-associated targets (TP53, STAT3, AKT1, HSP90AA1, TNF, IL-6, MAPK3, SRC, JUN, and HSP90AA1) as well as inflammation-related pathways (MAPK, HIF-1, Toll-Like Receptor, IL-17, TNF, and other signaling pathways). These mechanisms mitigate inflammation and reduce gastric mucosal damage in CAG mice.

In conclusion, TRCE was shown to alleviate CAG by modulating TP53, STAT3, AKT1, HSP90AA1, TNF, IL-6, MAPK3, SRC, JUN, and EGFR, as demonstrated by combined network pharmacology and biological experiments. In conclusion, our study provides a robust foundation for future clinical trials evaluating the efficacy of RC in treating CAG.

Gastric intestinal metaplasia (GIM) is a crucial stage in the progression of gastric cancer. Huangqi Jianzhong decoction (HQJZ) has emerged as a leading therapeutic strategy for treating GIM patients with cold intolerance in traditional Chinese medicine clinics, but the detailed mechanism remains poorly understood.

The present study aimed to elucidate the molecular mechanism by which HQJZ alleviates GIM in a rat model on the basis of the gut microbiota‒thyroid axis.

A GIM rat model was established by administering cold salicylic acid and sodium deoxycholate (SDC) for 12 weeks, followed by gavage treatment with HQJZ for an additional four weeks. Lianpu Yin (LPY) was used as a comparison formula. The cold tolerance characteristics of GIM rats were evaluated using cold tolerance and temperature‒tropism experiment experiments. Thyroid pathological changes were evaluated with HE staining, and thyroid function was measured via quantification of T3 and T4 levels with ELISA. The gut microbiota was analyzed using 16S rRNA gene sequencing, and fecal butyric acid and serum metabolites were quantified utilizing metabolomics. The key molecular mechanism was verified in the Nthy-ori 3-1 cell model.

HQJZ, but not LPY, significantly improved gastric mucosa and thyroid tissue lesions in GIM rats, increased the serum levels of the thyroid hormones T3 and T4, and enhanced cold tolerance. HQJZ treatment promoted the enrichment of fecal butyrate-producing bacteria, specifically the bacteria Allobaculum and Bifidobacterium, resulting in a marked increase in fecal butyric acid concentrations. HQJZ treatment significantly diminished the levels of mitochondrial damage-related serum metabolites, including p-cresol sulfate and indoxyl sulfate. Mechanistically, in vivo investigations further demonstrated that butyric acid not only improved thyroid tissue lesions but also restored the fecal microbiota structure, as well as low-temperature tropism, in GIM rats. Furthermore, butyrate diminished the mitochondrial damage induced by SDC in these cells, as evidenced by decreased reactive oxygen species levels and increased ATP production and mitochondrial membrane potential. Importantly, in vitro studies revealed that butyrate protected against SDC-induced injury in Nthy-ori 3-1 cells through the upregulation of TG, TPO, and TSHR expression.

HQJZ promotes cold tolerance and improves thyroid function in GIM rats by enriching gut butyrate-producing bacteria.

Identification of active components of traditional Chinese Medicine (TCM) and their respective targets is important for understanding the mechanisms underlying TCM efficacy. However, there are still no effective technical methods to achieve this.

Herein, we have established a method for rapidly identifying targets of a specific TCM and interrogating the targets with their corresponding active components based on Isothermal Shift Assay (iTSA) and database interrogation.

We optimized iTSA workflow and identified 110 targets for Danhong injection (DHI) which is used as an effective remedy for cardiovascular and cerebrovascular diseases. Moreover, we identified the targets of the nine major ingredients found in DHI. Database interrogation found that the potential targets for DHI, in which we verified that ADK as the target for salvianolic acid A and ALDH1B1 as the target for protocatechualdehyde in DHI, respectively.

Overall, we established a novel paradigm model for the identification of targets and their respective ingredients in DHI, which facilitates the discovery of drug candidates and targets for improving disease management and contributes to revealing the underlying mechanisms of TCM and fostering TCM development and modernization.

Chronic atrophic gastritis (CAG) is a chronic inflammatory disease and precancerous lesion in stomach cancer. Abnormal activation cellular ferroptosis further damages gastric tissue, which is susceptible to inflammation. Luteolin has powerful anti-inflammatory and regulatory potential for cellular ferroptosis. We aimed to clarify the involvement of luteolin in inflammation and ferroptosis during CAG. Luteolin targets were searched to identify intersecting genes in the chronic atrophic gastritis disease database. The AGE-RAGE pathway is a potential target of luteolin for the treatment of chronic atrophic gastritis and a binding site between luteolin and RAGE was predicted through a computer simulation of molecular docking. We established a CAG rat model using N-methyl-N-nitro-N-nitroguanidine. The therapeutic effect of luteolin on CAG was detected using western blotting, qPCR, hematoxylin and eosin staining, lipid oxidation (MDA), and Fe2+ assays. Luteolin inhibited the AGE-RAGE signaling pathway and reduced the inflammatory response in gastric tissues. Additionally, luteolin downregulated the concentration of (MDA) and Fe2+, and CAG downregulated the expression levels of ACSL4 and NOX1 and upregulated the expression levels of FIH1 and GPX4 ferroptosis-related proteins, thus inhibiting the ferroptosis of gastric tissue cells, which had a therapeutic effect on CAG.

Helicobacter pylori (H. pylori) plays a major role in causing and advancing gastrointestinal illnesses. Our aim is to analyze the unique makeup and functional changes in the gastric microbiota of patients with chronic non-atrophic gastritis (CNAG), regardless of the presence of H. pylori, and to determine the potential signaling pathways.

We performed metagenomic sequencing on gastric mucosa samples collected from 17 individuals with non-atrophic gastritis, comprising 6 cases were infected with H. pylori (H. pylori-infected case group) and 11 cases without (control group). The species composition was evaluated with DIAMOND software, and functional enrichment was assessed utilizing the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. We analyzed antibiotic resistance patterns using the Comprehensive Antibiotic Resistance Database as a reference (CARD).

The presence of H. pylori colonization in CNAG patients was associated with increased diversity in the gastric microbiota. The Phylum Firmicutes was found to be less prevalent, while the Phylum Proteobacteria showed an increase. Functionally, pathways associated with metabolic pathways, including vitamins, auxiliaries, amino acid residue, carbon hydrate, and metabolic energy pathways, were enriched in CNAG patients with H. pylori infection. Additionally, antibiotic resistance genes correlated with antibiotic efflux pump were enriched.

From a holistic genomic perspective, our findings offer fresh perspectives into the gastric microbiome among CNAG patients carrying H. pylori, which is valuable for future research on CNAG.

Chronic gastritis (CG) is a common gastrointestinal disorder characterized by inflammation of the stomach lining. Liver-stomach disharmony (LSD) syndrome is believed to contribute to CG symptoms.

To evaluate the efficacy and safety of microcosmic syndrome differentiation and Chinese herbal medicine (CHM) treatment in patients with CG and LSD syndrome.

Sixty-four patients with CG and LSD syndrome were randomly divided into two groups: The treatment group received CHM based on microcosmic syndrome differentiation and the control group received conventional Western medicine. The treatment course lasted 12 wk. The primary outcome was improvement in dyspeptic symptoms, measured using the Nepean Dyspepsia Index. The secondary outcomes included the improvement rate of endoscopic findings, histopathological findings, and microcosmic syndrome scores and the incidence of adverse events.

After 12 wk of treatment, the treatment group showed significantly greater improvement in dyspeptic symptoms than the control group (93.75% vs 65.63%, P < 0.01). The treatment group also showed a significantly higher improvement rate in endoscopic findings than the control group (81.25% vs 53.13%, P < 0.05). The improvement rates of histopathological findings and microcosmic syndrome scores were not significantly different between the two groups (P > 0.05). No serious adverse events were observed in either group.

Microcosmic syndrome differentiation and CHM treatment can effectively improve dyspeptic symptoms and endoscopic findings in patients with CG and LSD syndrome and have a good safety profile. Further studies with larger sample sizes and longer follow-up periods are required to confirm the long-term efficacy and mechanism of action of this treatment.

The progression from gastric mucosal inflammation to cancer signifies a pivotal event in the trajectory of gastric cancer (GC) development. Chinese medicine (CM) exhibits unique advantages and holds significant promise in inhibiting carcinogenesis of the gastric mucosa. This review intricately examines the critical pathological events during the transition from gastric mucosal inflammation-cancer transformation (GMICT), with a particular focus on pathological evolution mechanisms of spasmolytic polypeptide-expressing metaplasia (SPEM). Moreover, it investigates the pioneering applications and advancements of CM in intervening within the medical research domain of precancerous transformations leading to GC. Furthermore, the analysis extends to major shortcomings and challenges confronted by current research in gastric precancerous lesions, and innovative studies related to CM are presented. We offer a highly succinct yet optimistic outlook on future developmental trends. This paper endeavors to foster a profound understanding of forefront dynamics in GMICT research and scientific implications of modernizing CM. It also introduces a novel perspective for establishing a collaborative secondary prevention system for GC that integrates both Western and Chinese medicines.

Bian stone ironing and rubbing traditional Chinese medicine penetration method is based on the theory of regulating the middle and restoring balance. By using Bian stone to heat, ironing, and rubbing, pushing and rubbing in the epigastric area can regulate the spleen and stomach, restore the normal function of the middle jiao qi movement and the functions of the five organs. Bian stone hot ironing can harmonize stomach qi, nourish qi and assist yang, clear the internal organs and clear turbidity, regulate intestinal qi circulation, and promote qi stagnation.

The VAS score for stomach pain is 6 points, and the SAS score is moderate anxiety, which seriously affects sleep and daily life.

epigastric pain, spleen, and stomach deficiency cold syndrome.

Easy to digest diet, Western medicine provides famotidine acid inhibiting and protecting gastric mucosa, and mosapride promoting gastrointestinal peristalsis medication treatment; Traditional Chinese Medicine provides oral administration of Huangqi Jianzhong Tang and traditional Chinese medicine techniques such as Bianchi Ironing and Moxibustion for treatment.

The patient's symptoms of stomach pain have significantly improved, with a decrease in the epigastric pain score to 0, improved anxiety, reduced fatigue, improved sleep, improved epigastric fullness, unobstructed bowel movements, and improved quality of life. The patient is very satisfied.

The method of using Bian stone ironing and rubbing traditional Chinese medicine to treat stomach pain caused by the spleen and stomach deficiency cold can alleviate the symptoms of stomach pain in patients, and the improvement of symptoms shows a gradual increase, with significant effects. At the same time, it significantly improves patient anxiety and fatigue symptoms and can increase the sample size in future work to further clarify its clinical effects.

Background Commercial airline pilots (APs) are prone to upper gastrointestinal symptoms, such as epigastric pain and bloating. These issues are often linked to occupational risk factors like irregular diet, sleep disruption, and circadian rhythm disturbance. The use of probiotics to enhance intestinal health is well established, but their efficacy in treating upper gastrointestinal diseases is still debated. This is primarily due to the stomach's small resident microbiota and its low pH, which is inhospitable to most microbes. However, emerging research suggests that specific probiotic strains, such as Enterococcus faecium, can withstand acidic environments. Moreover, certain yeast species, including Saccharomyces boulardii, can survive at a low pH. Consequently, we conducted a preliminary, three-arm, randomized, open-label, dose-finding, four-week study to compare the effects of watchful waiting (WW) with the administration of an oral probiotic supplement containing S. boulardii and E. faecium in APs diagnosed with Helicobacter pylori-negative chronic non-atrophic gastritis (CNG). Methods The study included 39 APs with CNG who were randomized into three groups with a 1:1:1 ratio. The low-dose group (n = 13) received one capsule of the probiotic supplement twice daily, before meals, for four weeks. The high-dose group (n = 13) was administered two capsules of the supplement on the same schedule. The third group (n = 13) underwent WW and served as the control arm. Blinding was maintained for the examining physicians and laboratory staff, but not for the patients. All participants self-rated their experiences of gastric pain and bloating at the beginning and conclusion of the four-week treatment period. Additionally, serum levels of pepsinogen I (PGI) and pepsinogen II (PGII) were measured at these time points. Results Supplementation with probiotics significantly outperformed WW in reducing subjective gastric pain and bloating. This effect was consistent across both tested dosages, with no significant differences observed. However, only high-dose probiotics led to a statistically significant decrease in PGII levels and an increase in the PGI/PGII ratio after the four-week study period, a result not observed with low-dose probiotics. Conclusions Oral administration of S. boulardii and E. faecium demonstrated potential efficacy in reducing gastric pain and bloating symptoms in APs with CNG, as evidenced by statistically significant symptom improvement compared to the control group that did not receive the probiotic supplementation. Notably, high-dose probiotics resulted in a significant increase in the PGI/PGII ratio, indicating potential long-term cytoprotective effects on the gastric mucosa.