多途径干预TGF-β1对糖尿病大鼠主动脉血管平滑肌 p53、c-jun基因表达的作用_临床医学论文.docVIP

多途径干预TGF-β1对糖尿病大鼠主动脉血管平滑肌 p53、c-jun基因表达的作用_临床医学论文 多途径干预TGF-β1对糖尿病大鼠主动脉血管平滑肌 p53、c-jun基因表达的作用_临床医学论文 作者：向前,王芳,刘洪,王兰香,韩瑾 【摘要】 目的 探讨糖尿病大鼠主动脉中p53、c-jun基因mRNA表达及其TGF-β1抑制剂对其表达的影响。方法 链脲左菌素糖尿病大鼠随机分为对照组、联合干预组、维生素E组、氯沙坦、氨基胍组5组。联合干预组用Vitamin E［10 mg/（kg·d）］、Losartan［10 mg（kg·d）］、AG［50 mg/（kg·d）］，蒸馏水稀释至5 ml，一次性灌胃，对照组用5 ml蒸馏水，其他组按同样的方法分别处理，共饲养12周。用逆转录聚合酶链式反应检测基因的表达水平。结果 STZ大鼠主动脉中，p53、c-jun基因有明显的高表达，较正常组差异有显著性（0.05）。治疗12周后，p53、c-jun基因在实验组中表达明显减弱，与对照组差异有显著性（0.05）。结论 抑癌基因p53和原癌基因c-jun可能与糖尿病大鼠大血管病变有关，多途径干预TGF-β1可以抑制p53、c-jun基因表达，延缓大血管病变形成。 【关键词】 转移生长因子β1；p53基因；c-jun基因；糖尿病大鼠；血管并发症 Influence of mutiple inhibitors of TGF-β1 on p53,c-jun gene expression in aortic vascular smooth muscle of rats with diabetes ［Abstract］ Objective To study the expression of p53 and c-jun gene in the arteria maxima Galeni of streptozotocin（STZ）-induced diabetic rats,and the influence of the inhibitors of TGF-β1 on the mRNA expression.Methods Diabetic rats were randomly divided into 5 groups,they were contract group,combine interference,vitamin E group,losartan and aminoguanidine （AG）group.The interference group was taken orally once a day with 5ml solution which consisted of vitamin E［10 mg/（kg·d）］，losartan［10 mg/（kg·d）］and AG［50 mg/（kg·d）］.Contrast group was taken 5ml distilled water.Other groups were respectively taken vitamin E or losartan or aminoguanidine.The time was 12 weeks.The expression was examined by RT-PCR.Results P53 and c-jun gene expressed obviously in contrast group,which had evidently difference comparing to combine interference group（0.01）.There was no evidently difference among the 3 other groups,but their expression of p53 and c-jun gene was higher than combine group （0.05），but lower than contrast group（0.05）.Conclusion High expression of the p53 and c-jun gene in vascular may be have some matter with diabetic vascular complications; It can restrain the expression and delay the vascular complications by taken PKC,AR and AGEs inhibition. ［Key words］ transforming growth factor-beta1；