TLRs介导维药西帕依溃结安治疗溃疡性结肠炎机制研究

Ulcerative colitis is a chronic nonspecific intestinal inflammatory diseases, the real cause is still unclear.Traditional treatment can only temporary control and relieve symptoms, there are easy to relapse after drug withdrawal, long-term use can cause a lot of adverse reactions.Traditional Uyghur medicine KJA in accordance with treatment of the disease, curative effect, and less side effects, but the molecular mechanism of the effect is not clear.Experiments in this paper on the basis of preliminary experiment, using the uygur traditional prescription KJA intervention TNBS induced UC rat model.Observe different duration of general condition of rats, colon mucosa injury and inflammation for grading.Analysis of different duration of ulcerative colitis rats mesenteric lymph nodes in the dendritic cell phenotype and stimulate the change of the allogeneic T lymphocyte proliferation ability, immune footprint method and the real-time fluorescent quantitative PCR detected in rat colon TLR1, TLR2 and TLR6, MyD88, IFN - γ, IL - 1, IL - 6, the NF-κB, IL - 4, IL - 10 protein and mRNA expression.Compare Uyghur medicine KJA in accordance with the treatment effect, analysis of the mucosa of rats with the change of the system level of cytokine, explore the mechanism of drug , provide experimental basis for the rational use of drugs.

溃疡性结肠炎是一种慢性非特异性的肠道炎症性疾病，真正病因至今仍不清楚。传统治疗药物只能暂时的控制和缓解症状，存在着停药后易复发，长期应用会引起诸多不良反应的问题。传统维药西帕依溃结安治疗该病，疗效确切，且副作用少，但其作用的分子机理尚不清楚。本实验拟在前期实验的基础上，利用维医传统验方西帕依溃结安干预TNBS诱导的UC大鼠模型。观察不同用药时间大鼠一般状态，结肠粘膜损伤及对炎症进行评分。分析不同用药时间溃疡性结肠炎大鼠肠系膜淋巴结中树突状细胞表型及刺激同种异体T淋巴细胞增殖能力的变化，免疫印记法和实时荧光定量PCR分别检测大鼠结肠TLR1、TLR2、TLR6、MyD88、IFN-γ、IL-1、IL-6、NF-κB、IL-4、IL-10蛋白及mRNA的表达。比较维药西帕依溃结安的治疗效果，分析大鼠粘膜与系统水平细胞因子的变化，探讨药物作用机理，为维药西帕依溃结安的合理用药提供实验依据。

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