Abstract
BackgroundCinobufacini, the sterilized hot water extraction of dried toad skin, has been widely used in the treatment of inflammation and cancers. Recently we found cinobufacini could ameliorate dextran sulfate sodium (DSS)-induced colitis in mice, but the underlying mechanism was not fully understood. In current study, we explored the effect of cinobufacini on gut microbiota in DSS-induced acute colitic mouse model by pyrosequencing of colonic contents.MethodsC57BL/6 mice were supplied with normal or 3.0% DSS containing drinking water. DSS-treat mice were gavaged daily either with vehicle (water) or cinobufacini (10.0 or 30.0 mg/kg) for 7 days. The composition of the gut microbiota was assessed by analyzing 16S rRNA gene sequences.ResultsOur data indicated that cinobufacini reversed DSS-induced gut dysbiosis and enhanced intestinal barrier integrity. Moreover, changing of some specific microbial groups such as Proteobacteria and Bacteroides was closely correlated with the re-establishment of intestinal equilibrium and the recovery of intestinal function.ConclusionCinobufacini prevents colitis in mice by modifying the composition and function of gut microbiota. The current study provides additional mechanistic insight in the therapeutic effect of cinobufacini treatment and may pave the way for clinical application of cinobufacini in colitis therapy.
Highlights
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a heterogeneous group of chronic and relapsing inflammatory disorder of the gut
We explored the effect of cinobufacini on gut microbiota in dextran sulfate sodium (DSS)-induced acute colitic mouse model by pyrosequencing of colonic contents
The current study provides additional mechanistic insight in the therapeutic effect of cinobufacini treatment and may pave the way for clinical application of cinobufacini in colitis therapy
Summary
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a heterogeneous group of chronic and relapsing inflammatory disorder of the gut. A number of factors, such as immune function, genetics, and environmental factors such as smoking, antibiotics use, diet and so on, are associated with developing IBD[1]. Many of the known IBD susceptibility genes are associated with intestinal mucosal barrier function and are involved in host-microbiota interactions[4]. Other observations support a role for the gut microbiota in IBD including the use of faecal microbiota transplantation (FMT) as a therapeutic approach in IBD, and the rapidly increasing incidence of IBD globally associated with a Westernized lifestyle and other associated environmental factors[1,3,5,6]. We explored the effect of cinobufacini on gut microbiota in DSS-induced acute colitic mouse model by pyrosequencing of colonic contents
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