摘要
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.
AIM To develop a rat model of ulcerative colitis(UC)with abnormal sapra syndrome and detect the changes in inducible nitric oxide synthase(iNOS) and endothelial nitric oxide synthase(eNOS) hnRNA and mRNA expression in colon tissues of this model.METHODS Based on a rat model of abnormal sapra syndrome,trinitrobenzene sulfonic acid/ ethanol was used to induce UC in rats with abnormal sapra syndrome.Rats were randomly divided into two groups:normal group and UC with abnormal sapra syndrome model group.Quantitative RTPCR was used to detect the differences in iNOS and eNOS hnRNA and mRNA expression in colon tissues of rats in the two groups.RESULTS UC with abnormal sapra syndrome was successfully induced as evidenced by the presence of anticipated signs,symptoms and colonic mucosa damage.Compared with the normal group,the expression of iNOS hnRNA in colon tissue was significantly upregulated in the model group(P〈0.05),but the expression of eNOS hnRNA in colon tissue showed no statistical difference between the two groups(P〉0.05).The expression of iNOS and eNOS mRNA was significantly upregulated in the model group compared with the normal group(P〈0.05).CONCLUSION The inflammatory factors iNOS and eNOS are involved in the development of UC in rats with abnormal sapra syndrome,and changes in inflammation related factors are mediated by a post-transcriptional regulatory mechanism.
作者
阿地拉.阿不都艾尼
麦日排提.阿卜杜拉
卡思木江.阿西木江
张景萍
黄静静
布威阿依谢姆.依迪斯
哈力旦.阿布都
库热西.玉努斯
Adila·Abuduaini Mairipaiti·Abudula Kasimujiang·Aximujiang Jing-Ping Zhang Jing-Jing Huang Buweiayixiemu·Yidisi Halidan·Abudu Kurexi·Yunusi(Department of Biochemistry and Molecular Biology, School of Basic Medicine, Xinjiang Medical University, Urumqi 830011, Xinjiang Uygur Autonomous Region, China)
出处
《世界华人消化杂志》
CAS
2016年第36期4794-4804,共11页
World Chinese Journal of Digestology
基金
国家自然科学基金资助项目
No.81260564~~