摘要
目的:探讨苯那普利对糖尿病大鼠肾组织中转化生长因子β1(TGF-β1)和Smad7表达的影响。方法:将Wistar大鼠随机分为正常对照组、糖尿病非治疗组(模型组)和糖尿病苯那普利治疗组3组。用链脲佐菌素诱导造模。于给药8周后处死大鼠,检测各组大鼠的平均动脉压、血糖、肾功能指标、24h尿蛋白。采用逆转录多聚酶链反应(RT-PCR)检测TGF-β1及Smad7mRNA表达水平。采用免疫组化检测TGF-β1及Smad7蛋白定位的表达。结果:与正常组相比,糖尿病大鼠平均动脉压、血糖、肾功能指标、24h尿蛋白排出均增加;肾小球ECM明显增多、系膜区扩大(PAS染色);TGF-β1及Smad7mRNA表达上调;TGF-β1及Smad7蛋白的表达明显增加。苯那普利治疗后上述指标明显减轻。结论:TGF-β/Smad通路在糖尿病肾病时是激活的,苯那普利治疗可延缓肾脏损害。
Objective：To investigate the effect of Benazepril on expression of TGF- β1 and Smad7 in kidney tissue of diabetic rats, Methods： Healthy male Wistar rats were randomly divided into three groups： normal control group, diabetic rats group induced by strepotozocin and Benazepril - treated group, Rats were sacrificed after treatment for eight weeks. The mean arterial pressure, plasma glucose, BUN, Scr, urinary protein were observed, The level of TGF- β1 and Smad7 mRNA was examined by RT- PCR, The sites and level of TGF - β1 and Smad7 protein were examined by immunohistochemistry. Results：Compared to normal control group, mean arterial pressure, plasma glucose, BUN, Scr, 24h- urinary protein excretion significantly increased in diabetic rats group, which was associated with marked glomerular extracellular matrix accumulation and mesangial expansion（P_AS staining）, The level of TGF- β1 and Smad7 mRNA were up- regulated as well as the expression of TGF - β1 and Smad7 protein. Benazepril administration made all changes much better. Conclusion： TGF - β1 Smad signaling is activated in diabetic nephrology. Benazepril administration can attenuate renal damage in diabetic rats.
出处
《中国中西医结合肾病杂志》
2005年第10期569-572,共4页
Chinese Journal of Integrated Traditional and Western Nephrology
基金
河北省科技厅基金资助项目(No.05276101D-24)
