论文部分内容阅读
目的:研究贝那普利对糖尿病大鼠肾组织中TGF-β1和Smad4表达的影响。方法:用链脲佐菌素诱导的Wistar糖尿病大鼠为模型,随机分为N组、DM组和DM-B组3组,于给药8周后处死,检测各组大鼠的平均动脉压、血糖、肾功能指标及24小时尿蛋白。采用逆转录多聚酶链反应(RT-PCR)检测TGF-β1及Smad4mRNA表达水平。采用免疫组织化学方法检测TGF-β1及Smad4蛋白定位的表达,并用彩色病理图像分析系统进行定量分析。结果:与对照组相比,糖尿病大鼠平均动脉压、血糖、肾功能指标及24小时尿蛋白排出均增加;肾小球细胞外基质(ECM)明显增多、系膜区扩大(PAS染色);TGF-β1及Smad4mRNA表达上调;TGF-β1及Smad4蛋白的表达明显增加。贝那普利治疗后上述指标明显减轻(P<0·01)。结论:TGF-β/Smad通路在糖尿病肾病时是激活的,贝那普利治疗可延缓肾脏损害。
Objective: To study the effects of benazepril on the expression of TGF-β1 and Smad4 in the kidney of diabetic rats. Methods: The streptozotocin-induced Wistar diabetic rats as a model, were randomly divided into N, DM and DM-B groups were killed after 8 weeks of administration, the mean arterial pressure , Blood glucose, renal function and 24-hour urine protein. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of TGF-β1 and Smad4 mRNA. Immunohistochemistry was used to detect the expression of TGF-β1 and Smad4 protein, and quantitative analysis was performed by color pathological image analysis system. Results: Compared with the control group, mean arterial pressure, blood glucose, renal function and 24 - hour urinary protein excretion increased in diabetic rats. Glomerular extracellular matrix (ECM) increased and mesangial area enlarged (PAS staining). TGF-β1 and Smad4 mRNA expression increased; TGF-β1 and Smad4 protein expression increased significantly. The above indicators were significantly reduced after benazepril treatment (P <0.01). Conclusion: TGF-β / Smad pathway is activated in diabetic nephropathy, and benazepril treatment can delay renal damage.