Archives of physiology and biochemistry · 2026
Protective effect of quercetin on ulcerative colitis via p38 MAPK-MK2/MK3 signalling pathway: mechanism of anti-inflammatory cellular action.
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Zhang Jing, Wen Yongheng, Zhang Qiliang, Wang Yanrong, Shen Na, Guo Min, Zhou Zhiqian, Zhang Qiuzan
Аннотация
BACKGROUND: Ulcerative colitis is a chronic inflammatory bowel disease characterised by disrupted anti-inflammatory cell mechanisms in the intestinal mucosa.
PURPOSE: This study explores quercetin's protective role by restoring anti-inflammatory mechanisms and regulating this pathway.
METHODS: Experimental models included DSS-induced mice and LPS-stimulated RAW264.7 cells, assessed via disease activity scoring, histopathology, qPCR, ELISA, and Western blot.
RESULTS: Quercetin intervention could effectively repair the anti-inflammatory cell function, reverse the imbalance of inflammatory factors, inhibit the phosphorylation of p38 MAPK and the expression of MK2 and MK3, improve the intestinal mucosal damage and disease activity in mice, and reverse the pro-inflammatory polarisation of macrophages in vitro. Quercetin could further enhance the anti-inflammatory effect when combined with p38 MAPK inhibitor.
CONLUSION: Therefore, quercetin can repair the anti-inflammatory cell action mechanism, inhibit the activation of p38 MAPK-MK2/MK3 signalling pathway, alleviate the inflammatory damage of intestinal mucosa in ulcerative colitis, and provide experimental basis for anti-inflammatory cell-targeted treatment of ulcerative colitis.
PURPOSE: This study explores quercetin's protective role by restoring anti-inflammatory mechanisms and regulating this pathway.
METHODS: Experimental models included DSS-induced mice and LPS-stimulated RAW264.7 cells, assessed via disease activity scoring, histopathology, qPCR, ELISA, and Western blot.
RESULTS: Quercetin intervention could effectively repair the anti-inflammatory cell function, reverse the imbalance of inflammatory factors, inhibit the phosphorylation of p38 MAPK and the expression of MK2 and MK3, improve the intestinal mucosal damage and disease activity in mice, and reverse the pro-inflammatory polarisation of macrophages in vitro. Quercetin could further enhance the anti-inflammatory effect when combined with p38 MAPK inhibitor.
CONLUSION: Therefore, quercetin can repair the anti-inflammatory cell action mechanism, inhibit the activation of p38 MAPK-MK2/MK3 signalling pathway, alleviate the inflammatory damage of intestinal mucosa in ulcerative colitis, and provide experimental basis for anti-inflammatory cell-targeted treatment of ulcerative colitis.