European journal of pharmacology · 2026
Thymoquinone alleviates DSS-induced colitis in mice by protecting the intestinal mucosal barrier through inhibition of the Notch signalling pathway.
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Sun Tong, Tang Qiang, Xu Linxia, Liu Wei, Chen Fei, Zhang Xiaoling, Ren Zhi, Ma Zhenzeng, Zheng Hailun, Li Dapeng, Wang Qiangwu, Ke Xiquan
Аннотация
OBJECTIVE: To investigate the therapeutic effects and potential molecular mechanisms of the natural plant monomer thymoquinone (TQ) on colitis in mice. Particular attention was paid to protecting intestinal barrier integrity, apoptosis, and inflammatory responses.
METHODS: Colitis was induced in mice using 3% Dextran Sulfate Sodium (DSS). Concurrently, TQ (20 and 80 mg/kg) was administered intragastrically from days 1 to 7. The development of colitis and intestinal barrier integrity were assessed by monitoring body weight, Disease Activity Index (DAI) score, colonic length changes, pathological alterations, inflammatory cytokines, and the expression of relevant proteins. Caco-2 cells were stimulated in vitro with 100 ng/ml TNF-α to validate the regulatory effects of TQ on the Notch signaling pathway and tight junction proteins.
RESULTS: TQ significantly alleviates DSS-induced histopathological damage in mouse colon tissue, lowering the DAI. It reduces levels of pro-inflammatory cytokines (TNF-α, IL-1β) in peripheral serum, increases levels of the anti-inflammatory factor IL-10, and upregulates expression of intestinal barrier proteins (ZO-1, Occludin, MUC2). Furthermore, TQ upregulated Bcl-2, downregulated Bax, inhibited the activation of Cleaved Caspase-3, and reduced the apoptosis of mouse colonic epithelial cells. Mechanistically, TQ suppressed the excessive activation of the Notch signaling pathway, which is consistent with the results of the in vitro experiments.
CONCLUSION: TQ significantly alleviated the clinical manifestations and pathological damage in DSS-induced colitis in mice, protected the integrity of intestinal epithelial cells, and reduced apoptosis, demonstrating its potential as a novel therapeutic agent for inflammatory bowel disease (IBD).
METHODS: Colitis was induced in mice using 3% Dextran Sulfate Sodium (DSS). Concurrently, TQ (20 and 80 mg/kg) was administered intragastrically from days 1 to 7. The development of colitis and intestinal barrier integrity were assessed by monitoring body weight, Disease Activity Index (DAI) score, colonic length changes, pathological alterations, inflammatory cytokines, and the expression of relevant proteins. Caco-2 cells were stimulated in vitro with 100 ng/ml TNF-α to validate the regulatory effects of TQ on the Notch signaling pathway and tight junction proteins.
RESULTS: TQ significantly alleviates DSS-induced histopathological damage in mouse colon tissue, lowering the DAI. It reduces levels of pro-inflammatory cytokines (TNF-α, IL-1β) in peripheral serum, increases levels of the anti-inflammatory factor IL-10, and upregulates expression of intestinal barrier proteins (ZO-1, Occludin, MUC2). Furthermore, TQ upregulated Bcl-2, downregulated Bax, inhibited the activation of Cleaved Caspase-3, and reduced the apoptosis of mouse colonic epithelial cells. Mechanistically, TQ suppressed the excessive activation of the Notch signaling pathway, which is consistent with the results of the in vitro experiments.
CONCLUSION: TQ significantly alleviated the clinical manifestations and pathological damage in DSS-induced colitis in mice, protected the integrity of intestinal epithelial cells, and reduced apoptosis, demonstrating its potential as a novel therapeutic agent for inflammatory bowel disease (IBD).