论文摘要
目的:糖尿病肾病（Diabetic Nephropathy, DN）是糖尿病的主要晚期并发症之一,DN的病理改变如肾脏肥大、细胞外基质（extracellular matrix, ECM）的积聚等与转化生长因子β（transforming growth factor β, TGF-β）系统的启动有关。近年来,Smad蛋白家族被认为是一些TGF-β诱导基因的主要信号通路,其中TGF-β起转导作用。由于糖尿病造成了肾脏TGF-β系统的激活,故Smad通路可能在糖尿病阶段起作用。TGF-β配体与其受体TβRⅡ（transforming growth factor β receptor Ⅱ）结合后,激活TβRⅠ（transforming growth factor β receptor Ⅰ）受体的丝氨酸/苏氨酸激酶,Smad2、Smad3蛋白被磷酸化,活化的Smad2、Smad3才能与Smad4形成活性的转录复合物进入核内,调节相应的靶基因转录。许多研究显示,血管紧张素转化酶抑制剂（angiotensin converting enzyme inhibitor, ACEI）和血管紧张素受体拮抗剂（angiotensin receptor blocker, ARB）类药物可以下调TGF-β的表达。本研究主要观察糖尿病时大鼠肾脏TGF-β1、Smad4、Smad7的表达和定位及苯那普利、氯沙坦治疗对其的影响,为人类DN的早期防治提供实验性理论依据。 方法:用链脲佐菌素（strepotozocin, STZ）诱导的Wistar糖尿病大鼠为模型,随机分为正常对照组（N,n=12）,糖尿
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