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.
维普
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