Wogonoside alleviates ulcerative colitis-induced senescence by activating AMPK in in vivo and in vitro models

Ulcerative colitis (UC), a chronic inflammatory bowel disease, causes extensive damage, primarily affecting the colonic mucosa, where persistent inflammation leads to conditions such as mucosal congestion. Recent studies suggest a reciprocal interaction between intestinal cell senescence and inflammation; however, the connection between senescence and UC remains underexplored. Wogonoside, a key active component of Huangqin Decoction, has unclear effects on intestinal cell and tissue senescence in the context of UC.

Dextran Sodium Sulfate (DSS)-induced UC cell and animal models were employed to investigate the potential therapeutic effects of Wogonoside on intestinal epithelial cell senescence and its underlying mechanisms.

DSS treatment induced senescence in intestinal cells. Wogonoside alleviated senescence, as indicated by reduced levels of senescence markers (SA-β-gal, p16, p21, p53) and decreased epithelial damage, evidenced by increased occludin and ZO-1 expression. Mechanistic studies revealed that Wogonoside activates the AMPK signaling pathway, attenuating ROS production and thereby preventing intestinal cell senescence and injury. In vivo, Wogonoside similarly reduced DSS-induced senescence, as demonstrated by senescence marker analysis.

This study demonstrates that Wogonoside mitigates UC-induced intestinal cell senescence and epithelial barrier disruption by activating the AMPK pathway and reducing ROS production, offering protective effects in both cellular and animal models. These findings suggest that Wogonoside may be a promising therapeutic strategy for the treatment of UC.