Taxifolin is a bioflavonoid which has been used to treat Inflammatory Bowel Disease. However, taxifolin on DSS-induced colitis and gut health is still unclear. Here, we studied the effect of taxifolin on DSS-induced intestinal mucositis in mice. We measured the degree of intestinal mucosal injury and inflammatory response in DSS treated mice with or without taxifolin administration and studied the changes of fecal metabolites and intestinal microflora using 16S rRNA. The mechanism was further explored by fecal microbiota transplantation. The results showed that the weight loss and diarrhea score of the mice treated with taxifolin decreased in DSS-induced mice and longer colon length was displayed after taxifolin supplementation. Meanwhile, the expression of GPR41 and GPR43 in the colon was significantly increased by taxifolin treatment. Moreover, the expression of TNF-α, IL-1β, and IL-6 in colon tissue was inhibited by taxifolin treatment. The fecal metabolism pattern changed significantly after DSS treatment, which was reversed by taxifolin treatment. Importantly, taxifolin significantly increased the levels of butyric acid and isobutyric acid in the feces of DSS-treated mice. In terms of gut flora, taxifolin reversed the changes of Akkermansia, and further decreased uncultured_bacterium_f_Muribaculaceae. Fecal transplantation from taxifolin-treated mice showed a lower diarrhea score, reduced inflammatory response in the colon, and reduced intestinal mucosal damage, which may be related to the increased level of butyric acid in fecal metabolites. In conclusion, this study provides evidence that taxifolin can ameliorate DSS-induced colitis by altering gut microbiota to increase the production of SCFAs.

Ulcerative colitis (UC) is one of the primary types of inflammatory bowel disease, the occurrence of which has been increasing worldwide. Research in recent years has found that the level of lysozyme in the feces and blood of UC patients is abnormally elevated, and the bacterial product after the action of lysozyme can be used as an agonist to recognize different cell pattern receptors, thus regulating the process of intestinal inflammation. Berberine (BBR), as a clinical anti-diarrhea and anti-inflammatory drug, has been used in China for hundreds of years. In this study, results showed that BBR can significantly inhibit the expression and secretion of lysozyme in mice. Therefore, we try to investigate the mechanism behind it and elucidate the new anti-inflammatory mechanism of BBR. In vitro, lipopolysaccharide (LPS) was used to establish an inflammatory cell model, and transcriptomic was used to analyze the differentially expressed genes (DEGs) between the LPS group and the LPS + BBR treatment group. In vivo, dextran sulfate sodium salt (DSS) was used to establish a UC mice model, and histologic section and immunofluorescence trails were used to estimate the effect of BBR on UC mice and the expression of lysozyme in Paneth cells. Research results showed that BBR can inhibit the expression and secretion of lysozyme by promoting autophagy via the AMPK/MTOR/ULK1 pathway, and BBR promotes the maturation and expression of lysosomes. Accordingly, we conclude that inhibiting the expression and secretion of intestinal lysozyme is a new anti-inflammatory mechanism of BBR.

Early weaning is an effective method for improving the utilization rate of sows in intensive pig farms. However, weaning stress induces diarrhea and intestinal damage in piglets. Berberine (BBR) is known for its anti-diarrhea properties and ellagic acid (EA) is known for its antioxidant properties, however, whether their combination improves diarrhea and intestinal damage in piglets has not been studied, and the mechanism remains unclear. To explore the combined effects in this experiment, a total of 63 weaned piglets (Landrace × Yorkshire) were divided into three groups at 21 days. Piglets in the Ctrl group were treated with a basal diet and 2 mL saline orally, while those in the BE group were treated with a basal diet supplemented with 10 mg/kg (BW) BBR, 10 mg/kg (BW) EA, and 2 mL saline orally. Piglets in the FBE group were treated with a basal diet and 2 mL fecal microbiota suspension from the BE group orally, respectively, for 14 days. Compared with the Ctrl group, dietary supplementation with BE improved growth performance by increasing the average daily gain and average daily food intake and reducing the fecal score in weaned piglets. Dietary supplementation with BE also improved intestinal morphology and cell apoptosis by increasing the ratio of villus height to crypt depth and decreasing the average optical density of apoptotic cells; meanwhile, improvements also involved attenuating oxidative stress and intestinal barrier dysfunction by increasing the total antioxidant capacity, glutathione, and catalase, and upregulating the mRNA expressions of Occludin, Claudin-1, and ZO-1. Interestingly, the oral administration of a fecal microbiota suspension to piglets fed BE had similar effects to those of the BE group. According to 16S rDNA sequencing analysis, dietary supplementation with BE altered the composition of the microbiota, including firmicutes, bacteroidetes, lactobacillus, phascolarctobacterium, and parabacteroides, and increased the metabolites of propionate and butyrate. In addition, Spearman analysis revealed that improvements in growth performance and intestinal damage were significantly correlated with differential bacteria and short-chain fatty acids (SCFAs). In brief, dietary supplementation with BE improved the growth performance and intestinal damage by altering the gut microbiota composition and SCFAs in weaned piglets.