Administration of geniposide ameliorates dextran sulfate sodium-induced colitis in mice via inhibition of inflammation and mucosal damage

- Geniposide alleviated dextran sulfate sodium (DSS)-induced mice experimental colitis.
- Geniposide suppressed pro-inflammatory cytokines by regulating NF-κB and PPARγ pathways.
- Geniposide modulated DSS and LPS-induced decrease in the expression of ZO-1 and occludin.

Ulcerative colitis (UC), an idiopathic inflammatory bowel disease, not only affects millions of patients worldwide, but also increases the risk of colon cancer. Geniposide is an iridoid glycoside and has many biological activities such as anti-inflammatory and antioxidant. However, its protective efficacy and mechanism of action against UC are still unclear. In this study, we aimed to investigate the protective effects and mechanisms of geniposide on dextran sulfate sodium (DSS)-induced experimental colitis in mice. The results revealed that geniposide alleviated body weight loss, disease activity index, colon length shortening and colonic pathological damage induced by DSS. Geniposide significantly suppressed pro-inflammatory cytokines by regulating NF-κB and PPARγ pathways in vivo and in vitro. Furthermore, geniposide also significantly regulated the expressions of ZO-1 and occludin in DSS-induced experimental colitis in mice and lipopolysaccharide (LPS)-triggered inflammation in Caco-2 cells. These findings indicated that geniposide may be a new natural chemopreventive agent to combat UC.