贝那普利对阿霉素肾病大鼠肾脏保护作用的研究  

Protective Effect of Benazepril on the Progressive Injury of Podocyte in Rats with Adriamycin Nephropathy

作　　者：陈铖[1] 丁国华[1] 易家志[1] 朱玲[1] 

机构地区：[1]武汉大学人民医院肾内科,武汉430060

出　　处：《中国药师》2010年第9期1223-1225,共3页China Pharmacist

基　　金：国家自然科学基金资助项目(编号:30871167;30900688)

摘　　要：目的:观察贝那普利对阿霉素肾病大鼠形态学和肾皮质结蛋白表达改变的影响,探讨其对足细胞损伤的保护作用。方法:SD大鼠随机分为正常对照组、阿霉素肾病组和贝那普利治疗组。分别于给药4、7周后留取标本,检测24 h蛋白尿、血肌酐,肾组织行形态学检查,应用免疫组化法检测肾皮质中结蛋白表达。结果:肾病组大鼠尿蛋白排泄明显高于对照组(P<0.05),且有明显的肾小球足细胞损伤的病理学改变。肾皮质结蛋白表达增加(P<0.05)。贝那普利治疗后肾脏病理明显减轻,结蛋白表达降低(P<0.05)。结论:在阿霉素肾病中,贝那普利可改善肾小球足细胞的损伤程度,降低结蛋白表达,对肾小球起保护作用。Objective： To investigate the effect of benazepril on the expression of desmin in rat kidney cortex with adriamycin ne- phropathy （ADR） and the protective effect of benazepril on podocyte injury. Method： ADR model was created in Sprague-Dawley rats via tail vein injection of adriamycin（7.5 m g.kg^-1 ）. ADR animals were then treated with or without benazepril （ 10 mg.kg^-1 .d-1 ）. Serum creatinine and urinary protein were measured after 4 and 7 weeks. Expression of desmin protein was evaluated by immunohistochemistry respectively. Result： ADR rats had a significantly increase in desmin protein in the cortex when compared with control animals. ACE inhibition with benazepril significantly down-regulated desmin synthesis accompanied by an attenuation of glomerular injury. Conclusion： ACE inhibition with benazepril confers a protective effect on podocyte injury througl, down-regulation of desmin in adriamycin nephropathy.

关 键 词：贝那普利 阿霉素肾病 足细胞 结蛋白 

分 类 号：R965.1[医药卫生—药理学]