首页> 中文期刊> 《中国中西医结合肾病杂志》 >尾加压素Ⅱ在糖尿病肾病大鼠动脉粥样硬化形成的表达及黄芪的干预

尾加压素Ⅱ在糖尿病肾病大鼠动脉粥样硬化形成的表达及黄芪的干预

         

摘要

目的 观察糖尿病肾病大鼠主动脉、肾脏组织中尾加压素Ⅱ(urotensinⅡ,UⅡ)及其G蛋白耦联受体14(G-protein-coupled receptor14,GPR14)水平的变化,探讨UⅡ在糖尿病肾病动脉硬化形成的作用和发病机制及黄芪的干预效果.方法 采用高糖高脂饮食和链脲佐菌素(STZ)腹腔注射法建立大鼠糖尿病肾病模型.将大鼠分为正常对照组(NC)、糖尿病肾病组(DN)、黄芪治疗组(HZ)(予黄芪注射液5 ml/kg灌胃).于14周末处死动物,常规病理学检查,免疫组化观察UⅡ、GPR14蛋白表达;RT-PCR观察UⅡmRNA表达.结果 与NC组比较,DN组主动脉、肾组织UⅡ、GPR14表达增加,肾组织UⅡmRNA表达增加(P<0.01);与DN组比较,HZ组表达显著减少(P<0.05).结论 UⅡ及其受体GPR14的高表达提示其在糖尿病肾病动脉粥样硬化形成的过程中可能起重要作用;黄芪能够缓解肾脏病理损伤,其机制可能是通过抑制UⅡ和GPR14异常表达有关.%Objective: To observe the expression of urotensin Ⅱ(UⅡ ) and U II receptor G - protein - coupled receptorl4 ( GPR14 ) in the aorta and kidney of rats with diabetic nephropathy, so as to explore the function of U Ⅱ in diabetic nephropathy the formation of atherosclerosis and intervention of Astragalus. Methods; Rat model with diabetic nephropathy was established by high -carbonhydrate and high fat diet and intraperitoneal injection of streptozotocin( STZ ). The rats were randomly divided into 3 groups that is normal control group( NC),diabetic nephropathy group( DN), Astragalus treated group( HZ )( fed to the astragalus 5 ml/kg). Animals were sacrified at 14weeks, Pathology of renal tissues and thoracic aotra was examined. The expression of U Ⅱ -.GPR14 protein was detected by immunohistochemistry assay. The expression of U Ⅱ mRNA was measured by reverse transcription polymerase chain reac-tion( RT - PCR ). Results: Compared with NC group the expression of UⅡ and GPR14 protein were increased significantly in aorta and renal tissues of DN group( P < 0. 01 ). U ⅡI mRNA were increased significantly in renal tissues of DN group( P < 0. 01 ). However, the expression of UⅡ ,GPR14 protein and U Ⅱ mRNA in HZ group were significantly decreased in comparison with DN group( P <0. 05 ). Conclusion: UⅡ and its receptor GPR14 is highly expressed in diabetic nephropathy atherosclerosis formation may play animportant role. Astragalus can alleviate the damage of renal microvascular disease, which may be inhibiting abnormal expression of U II and GPR14 and play a role in renal protection.

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