ArticleAmerican journal of translational research2026
Wogonoside alleviates ulcerative colitis-induced senescence by activating AMPK in
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
methodsDextran 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.
resultsDSS 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.
conclusionThis 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.
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