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目的研究肾素-血管紧张素系统(RAS)对链脲佐菌素(STZ)诱导的糖尿病大鼠肾脏组织蛋白激酶C(PKC)α亚型的表达和转位的影响。方法将糖尿病模型大鼠随机分为伊贝沙坦组(40mg/kg)、福辛普利组(40mg/kg)、两药合用组(各20mg/kg)和糖尿病对照组。采用免疫组织化学法检测肾组织中PKCα的表达,采用Western blot法检测肾皮质、髓质PKCα的表达和胞膜转位情况。结果各用药组肾皮质PKCα总表达量和胞膜转位量均明显降低。各组间肾髓质PKCα的总量及胞膜、胞浆部分量的差异无显著性。结论RAS参与早期糖尿病大鼠肾脏中PKC途径,尤其是PKCα亚型的激活,而阻断RAS可部分纠正这种变化,提示RAS通过影响PKCα转导途径的异常参与糖尿病肾病的发生、发展机制。
Objective To investigate the effect of renin - angiotensin system (RAS) on the expression and translocation of PKCα in streptozotocin (STZ) - induced diabetic rats. Methods The diabetic rats were randomly divided into four groups: irbesartan group (40mg / kg), fosinopril group (40mg / kg), two combined groups (20mg / kg) and diabetic control group. Immunohistochemistry was used to detect the expression of PKCα in renal tissue. Western blot was used to detect the expression of PKCα in renal cortex and medulla. Results The total amount of PKCα expression and the amount of transmembrane translocation in the renal cortex of each treatment group were significantly decreased. There was no significant difference in the total amount of PKCα and the amount of membrane and cytoplasm in the medulla between groups. Conclusion RAS is involved in the activation of PKC pathway, especially in PKCα subtype in the kidney of early diabetic rats. Blockade of RAS may partially correct this change, suggesting that RAS may play an important role in the pathogenesis of diabetic nephropathy by affecting PKCα transduction pathway.