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[目的]评价清化肠饮对溃疡性结肠炎(UC)的治疗效果并阐明其可能的分子机制。[方法]利用葡聚糖硫酸钠(DSS)诱导UC小鼠模型,将动物随机分为3组:正常对照组、UC模型组和清化肠饮治疗组,每组各10只。观察小鼠疾病活动指数、组织病理学改变,测量血清淀粉酶样蛋白A(SAA)水平,以及观察清化肠饮对UC小鼠模型中TLR4、MyD88、IκB磷酸化表达水平,NF-κB核转录的影响。[结果]研究发现清化肠饮能够很好地改善DSS诱导UC小鼠模型的临床症状、结肠缩短和组织损伤。此外,经清化肠饮的治疗能明显降低DSS诱导的SAA的分泌。此外,清化肠饮能明显抑制DSS诱导的TLR4的表达和MyD88、IκB的磷酸化和NF-κB的核易位。[结论]抑制TLR4/NF-κB通路可能是清化肠饮治疗UC的机制之一。
[Objective] To evaluate the therapeutic effect of Qinghua Changyin on ulcerative colitis (UC) and elucidate its possible molecular mechanism. [Method] UC mouse model was induced by dextran sodium sulfate (DSS). The animals were randomly divided into 3 groups: normal control group, UC model group and Qinghua Changyin treatment group, with 10 mice in each group. The index of disease activity, histopathological changes and the level of serum amylase-like protein A (SAA) in mice were observed. The phosphorylation of TLR4, MyD88, IκB and the expression of NF-κB in UC mouse model were observed. The impact of transcription. [Results] The study found that Qinghua Decoction can effectively improve the clinical symptoms, colon shortening and tissue damage induced by DSS in UC mouse model. In addition, the treatment of Qinghai intestines can significantly reduce the DSS-induced SAA secretion. In addition, Qinghuachangyin significantly inhibited DSS-induced TLR4 expression and MyD88, IκB phosphorylation and NF-κB nuclear translocation. [Conclusion] Inhibition of TLR4 / NF-κB pathway may be one of the mechanisms of Qinghua Decoction in the treatment of UC.