中文摘要：

目的：探讨活性维生素D3对链脲佐菌素（STZ）诱导糖尿病肾病（DN）大鼠的肾保护作用是否与抑制瞬时受体电位阳离子通道蛋白6（TRPC6）有关.方法：30只雄性SD大鼠随机分为正常对照组（NC组）、DN组及DN加活性维生素D3干预组（DN＋ VD组）3组各10只.造模成功后6、12、18周检测大鼠体重、24 h尿蛋白量;造模成功后18周末处死大鼠,检测血样及肾组织指标变化.结果：DN＋ VD组与DN组相比蛋白尿显著减少,肾脏病理损伤改善.DN组与NC组比较,Podocin、Nephrin蛋白表达量均明显降低（均P＜0.05）,Desmin和TRPC6蛋白表达量均显著升高（均P＜0.05）,活性维生素D3干预后上述改变明显改善,差异有统计学意义.相关性分析显示：TRPC6与Podocin（r=-0.808,P＜0.05）、Nephrin（r=-0.791,P＜0.05）呈负相关,而与24 h尿蛋白（r=0.886,P＜0.05）、Desmin（r=0.929,P＜0.05）呈正相关.结论：活性维生素D3显著抑制STZ诱导的糖尿病大鼠肾脏损伤,其作用机制与调节足细胞TRPC6的表达有关.

英文摘要：

Objective：To investigate the protective effect of vitamin D3 on kidney in STZ-induced diabetic rats and its possible mechanism.Methods：Thirty male Spragam-Dawley rats were randomly divided into three groups：normal control（NC,n =10）,diabetic nephropathy（DN,n =10）,and DN treated with calcitriol（DN ＋ VD group,n =10）.DN model rats were established by intraperitoneal injections of STZ.Rats were sacrificed 18 w after treatment.Body weights were assessed and 24 h urine samples were collected in metabolic cages every6 w starting at 3 d after STZ injection.All animals were sacrificed at 18 w after treatment.At the end of the experiment and prior to sacrifice,blood samples were collected for biochemical studies,and the kidneys were used for histological assessments,immunohistochemical staining and western blot.Results：Pre-treatment of rats with vitamin D3 led to a significant attenuation proteinuric of rat experimental model of diabetes.This was associated with abrogation of disease associated induction of desmin and inhibition of TRPC6 expression.Vitamin D3 teatment up-regulation the expression of Nephrin and Podocin.Significant positive correlation was observed between TRPC6 and 24 h urinary protein （r =0.886,P ＜ 0.05）,Desmin （r =0.929,P ＜ 0.05） of podocyte injury maker.On the contrary,significant negative correlations were observed between TRPC6 protein and Nephrin expresion （r =-0.791,P ＜0.05） and Podocin （r =-0.808,P ＜ 0.05）.Conclusion：Vitamin D3 has protective effect on kidney in STZ-induced diabetic rats model,which might be related with the suppression of TRPC6 expresion.