Apigenin remodels the gut microbiota to ameliorate ulcerative colitis

Abstract

IntroductionUlcerative colitis (UC), a chronic non-specific colorectal inflammatory disease with unclear etiology, has long plagued human health. Gut microbiota dysbiosis destroy homeostasis of the colon, which is closely related to ulcerative colitis progress. Apigenin, a flavonoid widely present in celery, has been found to improve ulcerative colitis. However, the potential molecular mechanism of apigenin ameliorating ulcerative colitis through protecting intestinal barrier and regulating gut microbiota remains undefined.MethodsDextran sodium sulfate (DSS)-induced colitis mouse model was conducted to evaluate the effect of apigenin on UC. Disease activity index score of mice, colon tissue pathological, cytokines analysis, intestinal tight junction proteins expression, and colonic content short-chain fatty acids (SCFAs) and 16S rRNA gene sequencing were conducted to reflect the protection of apigenin on UC.ResultsThe results indicated that apigenin significantly relieved the intestinal pathological injury, increased goblet cells quantity and mucin secretion, promoted anti-inflammatory cytokines IL-10 expression, and inhibited the expression of proinflammatory cytokines, TNF-α, IL-1β, IL-6 and MPO activity of colon tissue. Apigenin increased ZO-1, claudin-1 and occludin expressions to restore the integrity of the intestinal barrier. Moreover, apigenin remodeled the disordered gut microbiota by regulating the abundance of Akkermansia, Turicibacter, Klebsiella, Romboutsia, etc., and its metabolites (SCFAs), attenuating DSS-induced colon injury. We also investigated the effect of apigenin supplementation on potential metabolic pathways of gut microbiota.ConclusionApigenin effectively ameliorated DSS-induced UC via balancing gut microbiome to inhibit inflammation and protect gut barrier. With low toxicity and high efficiency, apigenin might serve as a potential therapeutic strategy for the treatment of UC via regulating the interaction and mechanism between host and microorganism.

Compound chenpi tea consumption reduces obesity‐related metabolic disorders by modulating gut microbiota and serum metabolites in mice

“…It was reported that [ Eubacterium ]_ fissicatena _ group and Romboutsia were significantly increased in HFD‐fed mice and obese patients, and their high levels were positively correlated with body weight and serum lipids 19,20 . Romboutsia was also increased in esophageal cancer, ulcerative colitis, and diabetic retinopathy, suggesting that Romboutsia may be a potential pathogenic bacterium 21‐23 . Faecalibaculum is a proinflammatory bacterium, which is involved in exacerbating hepatic steatosis and damaging the intestinal barrier 24 .…”

“…19,20 Romboutsia was also increased in esophageal cancer, ulcerative colitis, and diabetic retinopathy, suggesting that Romboutsia may be a potential pathogenic bacterium. [21][22][23] Faecalibaculum is a proinflammatory bacterium, which is involved in exacerbating hepatic steatosis and damaging the intestinal barrier. 24 Correlation analysis showed that Faecalibaculum was positively correlated with TC and LDL-C. Gemella was significantly increased in obese patients and colon cancer patients.…”

Isoquercitrin alleviates lipopolysaccharide-induced intestinal mucosal barrier damage in mice by regulating TLR4/MyD88/NF-κB signaling pathway and intestinal flora

“…67 Noteworthily, numerous studies have shown that flavonoids can improve intestinal mucosal barrier damage by upregulating the expression of TJs and MUC2 mucin. 68,69 Thus, as a natural flavonoid compound, IQ is expected to protect the integrity of the intestinal mucosal barrier by enhancing the expression of TJs and mucins. In the present study, IQ treatment significantly increased the mRNA expression of ZO-1, Occludin, Claudin-1, and MUC2 in the ileum, revealing that IQ improved intestinal mucosal barrier damage induced by LPS…”

Egg yolk phosphatidylcholine alleviates DSS-induced colitis in BALB/c mice

“…34,49,62 It has been reported that DSS treatment increased the relative abundance of Proteobacteria in the intestines of mice. 63,64 The effects of EYPC on the abundance and composition of the gut flora were initially investigated. In contrast to previous studies, after two weeks of dietary EYPC supplementation, no significant difference was found in α-diversity between mice with colitis and those without EYPC supplementation, indicating that the anti-inflammatory effect of EYPC in this study was independent of changes in the diversity of gut microbiota.…”