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目的:观察小檗碱(Ber)对葡聚糖硫酸钠(DSS)所致结肠炎小鼠的疗效,并从内质网(ER)应激角度探讨其分子机制。方法:将30只小鼠随机分为正常对照(NOR)组、结肠炎模型(DSS)组和Ber治疗(DSS+Ber)组,每组10只。取小鼠远端结肠行病理切片,并进行肠道损伤评分;用Western blot方法测定小鼠结肠上皮细胞(IEC)中的ER应激标记物caspase-12和caspase-3的表达水平;用半定量RT-PCR方法测定ER应激标记物葡萄糖调节蛋白GRP78的mRNA表达水平。结果:给予DSS后小鼠出现典型的结肠炎变化。用Ber干预后,可显著降低结肠炎小鼠的结肠损伤评分,并可下调ER应激标记物caspase-12、caspase-3和GRP78 mRNA水平(P均<0.05)。结论:小檗碱可通过调节相关信号分子表达水平改善ER应激,减轻小鼠结肠炎性反应,保护肠道。
OBJECTIVE: To observe the therapeutic effect of berberine on mice with colitis induced by dextran sodium sulfate (DSS) and explore its molecular mechanism from the perspective of endoplasmic reticulum (ER) stress. Methods: Thirty mice were randomly divided into normal control (NOR) group, colitis model (DSS) group and Ber treated group (DSS + Ber), with 10 mice in each group. The pathological sections of the distal colon of mice were taken and the intestinal injury score was determined. The expression of ER stress markers caspase-12 and caspase-3 in mouse colonic epithelial cells (IEC) were determined by Western blot. Quantitative RT-PCR method was used to determine ER stress marker glucose regulation protein GRP78 mRNA expression levels. RESULTS: The mice developed typical colitis changes after DSS administration. The intervention of Ber could significantly reduce the colon injury score of colitis mice and down-regulate the expression of caspase-12, caspase-3 and GRP78 mRNA (all P <0.05). Conclusion: Berberine can improve the ER stress, regulate the colonic inflammatory response and protect the intestine by regulating the expression of related signaling molecules.