Deoxyschizandrin treats mice with ulcerative colitis possibly via the TLR4/NF-κB signaling pathway.

OBJECTIVE

This study aimed to investigate the effects and mechanisms of deoxyschizandrin (DSD) on treatment of ulcerative colitis (UC).

METHODS

The models of mice with UC were established through dextran sulfate sodium (DSS) administration, and the successful models were treated with DSD. The therapeutic effects of DSD on UC mice were evaluated and its behind mechanisms were analyzed.

RESULTS

After DSS induction, the mice showed increased body weight and colon length, worse disease activity index (DAI) and body inflammation, oxidative stress injury and increased apoptosis of colonic epithelial cells, which were remarkably relieved after DSD intervention. Besides, the levels of TLR4, MyD88 and NF-κB in the colon tissues were elevated in UC mouse models, while DSD treatment reduced the levels of these markers.

CONCLUSION

DSD can alleviate the symptoms of mice with DSS-induced UC via inhibiting body inflammation, improving oxidative stress and reducing the apoptosis of colonic epithelial cells, which may be attributed to DSD inhibition of the TLR4/NF-κB signaling pathway.