This study identified the chemical composition of Cyclocarya paliurus (Batal.) Iljinskaja flavonoids (CPF) and evaluated the antioxidant activities of 40% ethanol-eluted (EE)-CPF and 70% EE-CPF. Then we investigated whether 40% EE-CPF with stronger antioxidant capacity and higher flavonoid content exerted alleviative effects on dextran sulfate sodium (DSS)-induced colitis in mice. Our resulted showed that 40% EE-CPF improved colitis symptoms and colon tissue damage, as evidenced by the increased body weight, enhanced colon length, reduced disease activity index (DAI) score and increased goblet cells. Moreover, CPF reduced oxidative stress by regulating superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) levels, and restored intestinal barrier through Toll-like receptor 4(TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway, thereby exhibiting preventive effects on colitis in mice induced by DSS. Additionally, CPF regulated the composition of gut microbiota, leading to the increased beneficial microbiota, e.g., Lactobacillus and decreased harmful microbiota, e.g., Mucispirillum. Meanwhile, CPF increased the levels of short-chain fatty acids in cecal contents of mice. More interestingly, through microbiota functional analysis and correlation analysis, we proposed that CPF may alleviate colitis via microbial metabolism involved glycolysis Ⅲ and pyruvate fermentation pathways. Collectively, these results established a theoretical reference for developing CPF as anti-inflammatory agents in colitis.

Alcoholic liver disease (ALD) is thought to be primarily caused by oxidative damage and disruption of intestinal homeostasis. This study aimed to examine the protective effects of Chimonanthus salicifolius S. Y. Hu. leaves flavonoids (CLFs) against ALD and explore the underlying mechanisms based on hepatic oxidative stress, inflammation, intestinal barrier function and non-targeted metabolomics. The results indicated that CLFs improved the condition of mice with alcoholic liver disease and restored normal liver function. Through a combination of biochemical assays, non-targeted metabolomics, and gut microbiota analysis, we found that CLFs regulated glutathione metabolism and the tryptophan metabolic pathways, and activated the Nrf2/HO-1 signaling pathway, thus alleviating oxidative stress levels. Additionally, by regulating the composition of the gut microbiota and preserving intestinal barrier function, CLFs led to a decrease in harmful microorganisms like g-Sutterella and an increase in helpful microbes like g-Clostridium-f-Clostridiaceae. In summary, these findings provide a scientific basis for considering CLFs in the treatment of alcoholic liver disease.

Fibrillization endows food proteins with anisotropic nanostructures, significantly enhancing their functional properties. The resultant food protein fibrils (FPFs) have garnered attention for their diverse applications across the food industry. However, the full potential of FPFs is hindered by inherent challenges, particularly their limited stability. This review critically examines the formation of FPFs in food processing, the new protein sources, and on the modification strategies of FPFs, thereby unlocking new avenues for FPF utilization in food processing. In particular, the strategies during and after fibrillization are highlighted. The first strategy is to modify the structure and function of protein fibrils by influencing fibrillization, such as through pretreatment, incubation conditions, nuclei induction, and ingredient interactions. The second strategy is to modify the mature FPFs by regulating their properties and interactions with other components. The review also discusses the potential applications and challenges of FPFs in food systems, such as food preservation, functional food design, and novel delivery carriers.

Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease with a high incidence. Treatment for IBD includes medications and diet, and common anti-inflammatory medications have limitations like drug resistance and serious adverse effects. Accumulating evidence has demonstrated that dietary flavonoids exhibit an alleviative effect on IBD by influencing gut microbiota. The microbiota-derived metabolites also regulate IBD and maintain intestinal homeostasis. In this review, we investigate the therapeutic effect of gut microbiota and metabolites on IBD by intestinal immune and intestinal barrier function. We demonstrate the underlying mechanism of dietary flavonoids as an anti-inflammatory molecule alleviating IBD by regulating gut microbiota, short chain fatty acid (SCFA), bile acid (BA), tryptophan (Trp) metabolism and lipopolysaccharides (LPS)-toll-like receptor 4 (TLR4) signaling pathway. Based on structural differences of flavonoids, we summarize the recent research progress on the role of different dietary flavonoids in alleviating IBD by gut microbiota and metabolites in animal and clinical trials. This review indicates that dietary flavonoids targeting gut microbiota and metabolites provide a promising strategy for the treatment of inflammation and novel insights into the management of IBD.

Ferroptosis is a novel form of cell death driven by iron-dependent lipid peroxidation and it is implicated in various diseases, such as liver disease, acute kidney injury, cardiovascular disease, neurodegenerative disease and cancer. Lipid-based reactive oxygen species (ROS), particularly lipid hydroperoxides in the cellular membrane can lead to membrane disruption and cell death mediated by ferroptosis. There are three necessary stages involving in the process of lipid peroxidation regulation in ferroptosis, including the synthesis of membrane phospholipids, initiation of lipid peroxidation and clearance of lipid peroxides. In this review, we summarized the molecular modulation mechanisms of lipid peroxidation in ferroptosis from the above three stages, as well as various ferroptosis modulators targeting lipid peroxidation, including commonly used products, natural bioactive compounds and selenocompounds. Collectively, these findings suggest the vital role of lipid peroxidation in ferroptosis, and targeting lipid peroxidation in ferroptosis is potential to treat ferroptosis-associated diseases.

This study aimed to evaluate the alleviating effect of Chimonanthus nitens Oliv. leaves flavonoids (CLF) on hyperuricemia induced by potassium oxonate in mice. The results showed that CLF lowered the serum levels of uric acid (UA), creatinine and blood urea nitrogen, downregulated hepatic mRNA expressions of xanthine oxidase (XO), phosphate ribose pyrophosphate synthetase (PRPS) and adenosine deaminase (ADA) in hyperuricemia mice. In addition, CLF repaired renal injury by significantly down-regulating mRNA and protein expressions of renal UA reabsorption-related proteins and up-regulating the mRNA and protein expressions of UA secretory-related proteins. Finally, CLF inhibited UA synthesis and promoted UA excretion to alleviate hyperuricemia. Besides, CLF supplementation repaired the intestinal barrier function as demonstrated by significant increased mRNA levels of intestinal zonula occludens-1 (ZO-1), Occludin, mucin 2 (MUC2) and mucin 4 (MUC4), as well as decreased mRNA levels of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) in mice. Further research showed that CLF treatment restored intestinal homeostasis mediated by improving the composition of gut microbiota and elevating the abundance of beneficial bacteria like Lactobacillus, Alistipes, Prevotellaceae_UCG-001 and Parasutterella. Overall, our findings revealed a novel function of CLF as a promising therapeutic candidate for the treatment of hyperuricemia.