Effects of sodium butyrate on intestinal inflammation and composition of intestinal flora in rats with gastric ulcer
Objective To explore the effects of sodium butyrate(NaB)on intestinal inflammation and composition of in-testinal flora in rats with gastric ulcer so as to provide experimental evidence in the treatment of gastric ulcer with NaB.Methods SPF-level SD rats(6-8 weeks old,body mass:180-240 g)were randomly divided into normal group,model group,low-dose NaB group,high-dose NaB group and omeprazole group,8 cases in each group.The models of rats with gastric ulcer were constructed by hydrochloric acid+ethanol method.The rats in low-dose NaB group,high-dose NaB group and omeprazole group were given intragastric administration of 200 mg/kg NaB solution,400 mg/kg NaB solution and 20 mg/kg Omeprazole solution(once/d for 5 d),respectively.The gastric injury was evaluated,pathological changes of gastric mucosa were observed,the expressions of mucin 5AC(MUC5AC)and epidermal growth factor(EGF)in gastric mucosa were detected with fluorescence quantitative PCR,levels of serum interleukins(IL-6,IL-1β)and tumor necrosis factor α(TNF-α)were detected with ELISA,diversity of intestinal flora was detected by 16S rDNA high-throughput se-quencing method,and expressions of Toll-like receptor 4/nuclear factor κB(TLR4/NF-κB)signaling pathway related pro-teins were detected with Western blot.Results Compared with model group,gastric ulcer area,levels of serum IL-6,IL-1β and TNF-α,relative abundance of Proteobacteria,and expressions of TLR4 and NF-κB p65 in intestinal tissues were de-creased(all P＜0.05),while mRNA levels of MUC5AC and EGF,Shannon index of intestinal flora,relative abundance of Bacteroides and expression of nuclear factor κB inhibitor α(IκBα)were increased in low-dose NaB group,high-dose NaB group and omeprazole group(all P＜0.05).There were no significant difference in the above indexes between high-dose NaB group and omeprazole group(all P＞0.05).Conclusion NaB can significantly inhibit gastric ulcer,promote repair of gastric mucosa and improve intestinal flora disorders in rats,and its mechanism may be related to regulating TLR4/NF-κB signaling pathways and relieving inflammatory response.
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