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目的建立异常胆液质载体溃疡性结肠炎(ulcerative colitis,UC)病证大鼠模型,检测大鼠结肠组织中诱导型一氧化氮合酶(inducible nitric oxide synthase,i NOS)、内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)两种炎症相关因子,探讨他们在UC发生过程中的作用.方法将动物分为正常组和异常胆液质载体UC病证模型组,根据维医体液论,采用2,4,6-三硝基苯磺酸/乙醇法构建异常胆液质载体UC病证大鼠模型,应用实时荧光定量逆转录聚合酶链反应(quantitative real-time polymerase chain reaction,qRT-PCR)方法检测两组大鼠结肠组织中iNOS、eNOS的hnRNA与mRNA表达水平.结果 (1)异常胆液质载体UC病证模型组大鼠体征、症状、结肠黏膜损伤等均符合异常胆液质载体UC病证模型的判定标准;(2)qRTPCR结果显示,与正常组比较,异常胆液质载体UC病证模型组大鼠结肠组织中iNOS的hnRNA表达水平上调,差异有统计学意义(P<0.05),而eNOS的hnRNA表达水平无统计学意义(P>0.05);异常胆液质载体UC病证模型组大鼠结肠组织中iNOS、eNOS的mRNA表达水平均上调,差异有统计学意义(P<0.05).结论 (1)炎症相关因子iNOS、eNOS都参与了UC的发病过程;(2)异常胆液质载体UC病证大鼠结肠组织中炎症相关因子表达水平的调控存在mRNA的稳定性相关的转录后调控机制.
Objective To establish a rat model of abnormal bile ducts and ulcerative colitis (UC), to detect inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase To investigate the role of eNOS in the pathogenesis of UC.Methods The animals were divided into normal group and UC group with abnormal cholalocutaneous carrier, On the 2,4,6,6-trinitrobenzene sulfonic acid / ethanol method for the construction of abnormal choledochiocarcinoma UC rat model of disease, using real-time quantitative reverse-transcription polymerase chain reaction (quantitative real-time polymerase chain reaction, qRT-PCR) was used to detect the expression of iNOS and eNOS mRNA and protein in iNOS and eNOS of the two groups.Results (1) The signs, symptoms, colonic mucosal injury and so on were all consistent with abnormal UC (2) qRTPCR results showed that compared with the normal group, the abnormal expression of iNOS mRNA in colonic tissue of rats with abnormal bile-fluid-bearing UC syndrome model was up-regulated, the difference was statistically significant significance (P <0.05), but there was no significant difference in the expression of eNOS mRNA (P> 0.05). The mRNA expression of iNOS and eNOS in colonic tissue of UC patients with abnormal cholacitinoid UC model were all increased (P <0.05) .Conclusion (1) Inflammatory factors iNOS and eNOS are all involved in the pathogenesis of UC. (2) The regulation of inflammatory related factors expression in colonic tissues of abnormal bile-serum-bearing UC rats mRNA stability related post-transcriptional regulatory mechanisms.