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本文研究黄芩苷对葡聚糖硫酸钠(DSS)诱导的结肠炎小鼠模型的疗效,并从TLRs/MyD88通路探讨其作用机制。C57BL/6小鼠24只,分为空白对照组、模型组和黄芩苷组,用3.5%DSS诱导结肠炎模型,黄芩苷(30 mg/kg)干预7天,记录小鼠的疾病活动指数(DAI)评分,HE染色观察病理改变并评分,检测结肠髓过氧化物酶(MPO)活性,ELISA法检测肿瘤坏死因子(TNF)-α和白介素(IL)-6浓度,Real-time PCR法检测TLR2、TLR4和MyD88 mRNA表达水平。结果显示黄芩苷能有效抑制结肠炎小鼠DAI评分、结肠组织病理学评分和MPO活性,降低IL-6和TNF-α表达,降低TLR2、TLR4和MyD88 mRNA的表达。表明黄芩苷能有效缓解DSS诱导的结肠炎小鼠模型的症状,降低炎症反应,其作用机制可能是与TLRs/MyD88通路相关。
This article studies the efficacy of baicalin on dextran sodium sulfate (DSS) -induced colitis in mice and explores its mechanism of action from the TLRs / MyD88 pathway. Twenty-four C57BL / 6 mice were divided into blank control group, model group and baicalin group. The model of colitis induced by 3.5% DSS and the intervention of baicalin (30 mg / kg) for 7 days were recorded. The disease activity index DAI). The pathological changes were observed by HE staining and the scores of MPO were measured. The concentrations of tumor necrosis factor (TNF) -alpha and interleukin-6 (IL-6) were measured by ELISA. Real-time PCR TLR2, TLR4 and MyD88 mRNA expression levels. The results showed that baicalin can effectively inhibit the colitis mice DAI score, colon histopathological score and MPO activity, reduce the expression of IL-6 and TNF-α, reduce TLR2, TLR4 and MyD88 mRNA expression. The results showed that baicalin can effectively alleviate the symptoms of DSS-induced colitis mouse model and reduce the inflammatory reaction, and its mechanism may be related to the TLRs / MyD88 pathway.