Mechanism of ursodeoxycholic acid combined with bifid triple viable in the treatment of experimental colitis in mice

Objective To investigate the mechanism of ursodeoxycholic acid, bifid triple viable and their combination in the treatment of experimental colitis induced by dextran sulfate sodium (DSS) in mice. Methods Mice were divided into eight groups: a control group, a model (DSS) group, a ursodeoxycholic acid (UDCA1) group (30 mg×kg^-1×d^-1) and a (UDCA) group (260 mg×kg^-1×d^-1), a Bifid group (2.010¹⁰CFU/L), two combination groups (Bifid+UDCA1 and Bifid+UDCA2) and a positive control sulfasalazine (Sulfa) group (200 mg×kg^-1×d^-1). Except the control group, other groups were given 3.5% DSS solution for 7 days to establish an acute colitis model. The corresponding drugs were given to different groups, and the disease activity index (DAI) was recorded every day. The colon length was measured after administration. HE staining was used to evaluate the histological changes of each group. Western Blot was used to detect the levels of pathogen associated molecular pattern recognition receptors toll like receptor 4 (TLR4) and cascade induced nuclear factor-κB p65 (NF-κB p65) and the bile acids receptor farnesoid X receptor (FXR) in the colonic tissues. Results Compared with those exposed to UDCA or Bifid alone, the combination groups presented remarkable decreases in DAI, increases in colon length, and decreases in histopathological score (P<0.05); decreases in the levels of TLR4, and NF-κB p65 (P<0.05); and increases in the level of FXR (P<0.05). Conclusions The UDCA2 group, the Bifid group and their combination group can effectively alleviate experimental colitis in mice, while the combination group can better regulate the intestinal mucosal barrier function, intestinal microorganisms and bile acids metabolism, with better therapeutic effects on mice with experimental colitis.