盐酸贝那普利对早期糖尿病大鼠肾组织足糖萼蛋白表达的影响

目的观察盐酸贝那普利对早期糖尿病大鼠肾组织足糖萼蛋白(PCX)表达的影响,初步探讨其对糖尿病大鼠肾脏保护作用及其可能的机制。方法将健康雄性SD大鼠随机分为正常对照(NC)组和实验组。实验组大鼠一次性腹腔注射链脲佐菌素(STZ)建立糖尿病大鼠模型。造模成功后,随机分为糖尿病(DM)组和盐酸贝那普利干预(DT)组,每周检测各组大鼠血糖。4周后,检测大鼠尿白蛋白(UALB)、尿视黄醇结合蛋白(URBP)、尿足细胞特异性标志蛋白PCX(UPCX)、尿肌酐(UCR)、肾脏肥大指数(KI)及糖化血红蛋白(HbA1C)。采用免疫组化及RT-PCR法检测肾脏组织PCX蛋白及mRNA的表达。结果 DM组大鼠血糖、UALB、URBP、UPCX、KI、HbA1C均高于NC组(P<0.01),肾组织病理改变较重,肾组织PCX蛋白及mRNA的表达显著降低(P<0.01);DT组除血糖及HbA1C外,生化指标均明显低于DM组(P<0.01),肾组织病理改变亦减轻,肾组织PCX蛋白及mRNA的表达显著增高(P<0.01)。结论 PCX表达减少可能是糖尿病肾病发病机制之一,盐酸贝那普利可通过减轻尿液PCX排泄,上调肾组织PCX蛋白及mRNA的表达。

Effect of hydrochloride benazepril on Podocalyxin expression in diabetic rats

Objective To observe the effects of hydrochloride benazepril on the podocalyxin(PCX) protein expression in kidney of diabetic rats at early stages,and investigate its protective effect on the kidneys of diabetic rats and other possible related mechanisms.Methods Healthy Sprague-Dawley(SD) male rats were divided into the normal control(group NC) and the model group,then streptozotoin(STZ)-induced diabetic model rats were treated with(group DM) or without hydrochloride benazepril(group DT).Blood glucose was measured weekly in all groups.At the end of the 4th week,urinary albumin(UALB),urinary retinol binding protein(URBP),urinary podocyte-specific marker proteins PCX(UPCX),urinary creatinine(UCR) and glycated hemoglobin(HbA1C) were measured.PCX protein and mRNA expression in renal tissues were measured by immunohistochemistry and RTPCR.Results At the end of the 4th week,compared with group NC,BG,HbA1C,UALB,URBP,UPCX,KI were markedly increased in group DM(P < 0.01),the renal PCX protein and mRNA expression of kidney were significantly decreased(P < 0.01),the renal pathological lesions of rats in group DM were obvious.Compared with group DM,except for BG and HbA1C,the rest indexes were significantly decreased(P < 0.01),the renal pathological lesions of rats in group DT were less,the renal PCX protein and mRNA expression of kidney were significantly raised(P < 0.01).Conclusion Hydrochloride benazepril can reduce the excretion of PCX in urine,and stimulate the PCX protein and mRNA expression of kidney,which may be one of mechanisms of diabetic nephropathy.