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.