Baicalin is reported as an effective
drug for
ulcerative colitis (UC). However, its effect on gut microbiota and
short-chain fatty acids (SCFAs) remains unknown. In this study, we investigated the role of
baicalin on Th17/Treg balance, gut microbiota community, and SCFAs levels in trinitrobenzene sulphonic
acid (TNBS)-induced UC rat model. We found the DAI scores were significantly increased in the TNBS-treated rats, while reduced in the
baicalin-treated group in a dose-dependent manner, accompanied with the alleviation of mucosal injury, the reduction of ZO-1,
Occludin, and MUC2 expression. At the meanwhile,
baicalin repressed the increased levels of
reactive oxygen species (ROS) and MDA, while deceased the GSH and SOD levels in colon tissue of rats treated with TNBS. On the other hand, administration of
baicalin attenuated the TNBS-induced upregulations of Th17/Treg ratio, indicating a strong amelioration in the colorectal
inflammation. More importantly, pyrosequencing of the V4 regions of
16S rRNA genes in rat feces revealed a deviation of the gut microbiota in response to
baicalin treatment. In particular, the decreased Firmicutes-to-Bacteroidetes ratios and
endotoxin-bearing Proteobacteria levels indicated that
baicalin reversed TNBS-induced gut
dysbiosis OTUs. In addition, we further investigated the fecal levels of major SCFAs in rats and found that
baicalin significantly resorted the fecal
butyrate levels in rats treated with TNBS. The increased
butyrate levels were in consistent with the higher abundance of
butyrate-producing species such as Butyricimonas spp., Roseburia spp., Subdoligranulum spp., and Eubacteriu spp. in
baicalin-treated group. In conclusion, our findings suggest that
baicalin possibly protected rats against
ulcerative colitis by regulation of Th17/Treg balance, and modulation of both gut microbiota and SCFAs.
Baicalin may be used as a
prebiotic agent to treat
ulcerative colitis-associated
inflammation and gut
dysbiosis.