The food industry has been focusing on food bioactive compounds with multiple physiological and immunological properties that benefit human health. These bioactive compounds, including polyphenols, flavonoids, and terpenoids, have great potential to limit inflammatory responses especially NLRP3 inflammasome activation, which is a key innate immune platform for inflammation. Current studies have revealed numerous food bioactive compounds with promising activities for unraveling immune metabolic disorders and excessive inflammatory responses by directly and indirectly regulating the NLRP3 inflammasome activation. This review explores the food hazards, including microbial and abiotic factors, that may trigger NLRP3-mediated illnesses and inflammation. It also highlights bioactive compounds in food that can suppress NLRP3 inflammasome activation through various mechanisms, linking its activation and inhibition to different pathways. Especially, this review provided further insight into NLRP3-related targets where food bioactive compounds can interact to block the NLRP3 inflammasome activation process, as well as mechanisms on how these compounds facilitate inactivation processes.

Maxim is a traditional ethnic medicine commonly used in Tibet. In Tibetan medicine theory, Lagotis brachystachya is mainly used for the treatment of inflammatory related diseases. However, the active components and mechanism of the anti-inflammatory activity of Lagotis brachystachya are not clear.

The putative anti-inflammatory active compounds from Lagotis brachystachya Maxim and its anti-inflammation related mechanism involving in the TLR4/MyD88/NF-κB and NLRP3 signaling pathways were investigated.

In this study, we investigated the anti-inflammatory activity and mechanism of 32 compounds extracted from Lagotis brachystachya in HepG2 and THP-1 cells using the alcohol-induced HepG2 cell injury model and the monosodium urate (MSU) combined with lipopolysaccharide (LPS)-induced THP-1 cell inflammation model.

The results found that six compounds, including Echinacoside, Quercetin, Homoplantaginin, Tricin-7-O-glucoside, Apigenin and Luteolin-7-O-beta-d-glucopyranoside, were shown to exhibit significant anti-inflammatory effects in both cell models. Furthermore, these compounds were shown to inhibit the TLR4/MyD88/NF-κB and NLRP3 signaling pathways and reduce the release of pro-inflammatory cytokines IL-1β, TNF-α, and IL-6 in both cell models.

These findings suggest that Echinacoside, Quercetin, Homoplantaginin, Tricin-7-O-glucoside, Apigenin and Luteolin-7-O-beta-d-glucopyranoside from Lagotis brachystachya have promising potential as natural anti-inflammatory agents for the treatment of inflammatory-related diseases. The discovery of bioactive compounds from this plant opens up possibilities for the development of novel treatments for inflammatory-related diseases, potentially providing alternative or adjunctive options to conventional therapies.

Cancer continues to increase global morbidity and mortality rates. Despite substantial progress in the development of various chemically synthesized anti-cancer drugs, the poor prognosis of the disease still remains a big challenge. The most common drawback of conventional cancer therapies is the emergence of drug resistance eventually leading to the discontinuation of chemotherapy. Moreover, advanced target-specific therapies including immunotherapy and stem cell therapy are expensive enough and are unaffordable for most patients in poorer nations. Therefore, alternative and cheaper therapeutic strategies are needed to complement the current cancer treatment approaches. Phytochemicals are bioactive compounds produced naturally by plants and have great potential in human health and disease. These compounds possess antiproliferative, anti-oxidant, and immunomodulatory properties. Among the phytochemicals, flavonoids are very effective in treating a wide range of diseases from cardiovascular diseases and immunological disorders to cancer. They scavenge reactive oxygen species (ROS), inhibit cancer metastasis, modulate the immune system and induce apoptotic or autophagic cell death in cancers. This review will discuss the potential of various phytochemicals particularly flavonoids in attempts to target various cancers.

Environmental pollution is changing with economic development. Most environmental pollutants are characterized by stable chemical properties, strong migration, potential toxicity, and multiple exposure routes. Harmful substances are discharged excessively, and large quantities of unknown new compounds are emerging, being transmitted and amplifying in the food chain. The increasingly severe problems of environmental pollution have forced people to re-examine the relationship between environmental pollution and health. Pyroptosis and activation of the NLRP3 inflammasome are critical in maintaining the immune balance and regulating the inflammatory process. Numerous diseases caused by environmental pollutants are closely related to NLRP3 inflammasome activation and pyroptosis. We intend to systematically explain the steps and important events that are common in life but easily overlooked by which environmental pollutants activate the NLRP3 inflammasome and pyroptosis pathways. This comprehensive review also discusses the interaction network between environmental pollutants, the NLRP3 inflammasome, pyroptosis, and diseases. Thus, research progress on the impact of decreasing oxidative stress levels to inhibit the NLRP3 inflammasome and pyroptosis, thereby repairing homeostasis and reshaping health, is systematically examined. This review aims to deepen the understanding of the impact of environmental pollutants on life and health and provide a theoretical basis and potential programs for the development of corresponding treatment strategies.

Pyroptosis plays an important role in inflammatory diseases such as viral hepatitis and atherosclerosis. Apigenin exhibits various bioactivities, particularly anti-inflammation, but its effect on pyroptosis remains unclear. The aim of this study is to investigate the effect of apigenin on pyroptosis and explore its potential against inflammatory diseases. THP-1 macrophages treated by lipopolysaccharides/adenosine 5'-triphosphate were used as the in vitro pyroptosis model. Western blot was used to detect the expression of NLRP3 inflammasome components and key regulators. Immunofluorescence was used to observe ROS production and intracellular location of p65. The potential of apigenin against inflammatory diseases was evaluated using atherosclerotic mice. Plaque progression was observed by pathological staining. Immunofluorescence was used to observe the expression of NLRP3 inflammasome components in plaques. The results showed that apigenin inhibited NLRP3 inflammasome activation. Apigenin reduced ROS overproduction and inhibited p65 nuclear translocation. Additionally, apigenin decreased the expression of NLRP3 inflammasome components in the plaque. Plaque progression was inhibited by apigenin. In conclusion, apigenin exhibited a preventive effect on macrophage pyroptosis by reducing oxidative stress and inhibiting the NF-κB pathway. Apigenin may alleviate atherosclerosis at least partially by inhibiting macrophage pyroptosis. These findings suggest apigenin to be a promising therapeutic agent for inflammatory diseases.

Bioactive compounds, such as carotenoids, alkaloids, and phenolics, are well known because of their alleged health benefits when consumed regularly in a balanced healthy diet. Some well-documented bioactivities are antioxidant, antihypertensive, antihyperglycemic, antilipidemic, anti-obesity, anti-inflammatory, and antimicrobial capacities. Trying to associate the chemical composition of distinct sources and their bioactivity using in vitro methods, several assays have been developed, implemented, and optimised to recapitulate human physiological conditions. However, in most cases, pitfalls are apparent, and no single test tube-based assay can predict in vivo responses. The need for a more physiologically relevant cell-based method to evaluate the antioxidant capacity of putative antioxidants is apparent. Therefore, in this Review, the current state-of-the-art in food science and nutrition is aligned with cell biology/bioengineering approaches to propose combining in vitro digestion and absorption to obtain a bioavailable fraction containing antioxidants. Overall, human plasma, 2-dimensional human cell lines, such as erythrocytes, lymphocytes, hepatocytes, enterocytes and, ultimately, 3-dimensional spheroids (organoids) could be used as biologically relevant models to assess the antioxidant activity of compounds, foods, and nutraceuticals. This versatile approach is deemed suitable, accurate, reproducible, and physiologically relevant to evaluate the protective effects of antioxidants against ROS-mediated oxidation in vitro.

Avermectin pollution is an important problem that cannot be ignored in aquatic system in recent years. It has brought great trouble to freshwater aquaculture, especially fishery aquaculture. Plant-derived quercetin has anti-inflammatory and antioxidant properties and is widely used as a dietary additive, but its protective effect on immune damage induced by avermectin in freshwater carp remains unclear. This study evaluated the role of dietary additive quercetin supplementation in chronic avermectin exposure of carp spleen. Sixty carp were divided into 4 groups (n = 15/ group), including control group, avermectin treatment group, quercetin treatment group, quercetin and avermectin co-treatment group. Carp were exposed to a 1/10 96 h LC₅₀ dose of avermectin for 30 d and fed a carp diet containing 400 mg/kg quercetin twice a day (3% body weigh/ carp). The results showed that chronic avermectin exposure caused the loose parenchymal structure of carp spleen tissue and the increase of inflammatory cells, accompanied by increased transcription levels of pro-inflammatory il-1β, il-6, tnf-α and decreased levels of anti-inflammatory factors il-10 and tgf-β1, ROS accumulation in spleen tissue. MDA content increased and T-AOC, CAT and GSH levels decreased. Quercetin down-regulates the NF-κB pathway by inhibiting the expression of iNOS and activating p38 MAPK, blocking the transcription of inflammatory factors, and alleviating the inflammation of carp spleen caused by chronic avermectin exposure. In addition, quercetin inhibits the over-activation of Nrf2/Keap-1 signaling axis, blocks ROS accumulation, and restores the spleen REDOX homeostasis. In conclusion, quercetin, as a dietary additive for carp feed, can effectively improve the immune damage caused by avermectin pollution in aquatic environment, resist spleen inflammation and oxidative stress, and provide a theoretical basis for clinical development of freshwater carp feed.

Glycidol is a well-known food contaminant mainly formed in refined edible oils and various thermally processed foods. Here, we studied the toxicity effects and related mechanism of glycidol on Human umbilical vein endothelial cells (HUVECs). Glycidol was found to induce Gap period 2 (G2)/Mitosis (M) phase cell cycle arrest, apoptosis, and autophagy in HUVECs. Inhibition of autophagy by 3-methyladenine (3-MA) attenuated glycidol-induced cell death, suggesting that glycidol-induced apoptosis was autophagy-dependent. Moreover, glycidol treatment induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal protein kinase (JNK), and p38. Inhibition of ERK, JNK, and p38 phosphorylation by the inhibitors U0126, SP600125, and SB203580 attenuated glycidol-induced autophagy and prevented glycidol-mediated reduction in cell viability, demonstrating that glycidol inhibited HUVECs growth by inducing autophagic-dependent apoptosis through activation of the ERK, JNK and p38 signaling pathways. In addition, apigenin (API) and its octoic acid diester apigenin-7 (API-C8), 4'-O-dioctanoate were found to significantly attenuate glycidol-induced cell growth inhibition by inhibiting the above signaling pathways. Collectively, glycidol induces autophagic-dependent apoptosis via activating the ERK/JNK/p38 signaling pathways in HUVECs and API-C8 could attenuate the toxicity effects.

Home cooking has been considered as an indoor pollution problem since cooking oil fumes contain various toxic chemicals such as aldehydes. Fortifying edible oils with docosahexaenoic acid (DHA) has been applied to enhance the nutritional value of oils. This study designed a frying simulation system and examined the effect of oil type, DHA fortification, heating time, and addition of natural antioxidant on the emissions of aldehydes from heated oils. Results showed that linseed oil had the highest total aldehyde emissions, followed by soybean oil, peanut oil, and palm oil. Fortifying soybean oil with DHA increased the toxic aldehydes emitted. Quercetin, a flavonoid, significantly reduced aldehydes emitted from DHA-fortified soybean oil (by up to 39.80%) to levels similar to those of normal soybean oil. Further analysis showed that DHA-fortified soybean oil with quercetin had a significantly higher DHA and unsaturated fatty acids (UFAs) content than the control oil at each heating time point. The result indicated that quercetin inhibited emissions of aldehydes, at least in part, by protecting UFAs from oxidation. Collectively, quercetin could be used as a natural additive in DHA-fortified and normal cooking oils to reduce aldehyde emissions, indoor air pollution, and preserve functional DHA and other UFAs.

Advanced glycation end products (AGEs) are generated by the nonenzymatic glycation of proteins or lipids. Diabetic retinopathy (DR) is one common complication in patients with diabetes. The accumulation of AGEs in retinal cells is strongly associated with the development of DR. AGEs can induce the breakdown of redox balance and then cause oxidative stress in retinal cells, exerting cytopathic effects in the progression of DR. The interaction between AGEs and the receptor for AGE (RAGE) is involved in multiple cellular pathological alterations in the retina. This review is to elucidate the pathogenetic roles of AGEs in the progression of DR, including metabolic abnormalities, lipid peroxidation, structural and functional alterations, and neurodegeneration. In addition, disorders associated with AGEs can be used as potential therapeutic targets to explore effective and safe treatments for DR. In this review, we have also introduced antioxidant phytochemicals as potential therapeutic strategies for the treatment of DR.