摘要
目的:研究抑制肾素-血管紧张素系统(RAS)对糖尿病大鼠心脏蛋白激酶C-alpha(PKCα),蛋白激酶C-betaⅡ(PKCβⅡ)表达的影响,探讨抑制RAS减少糖尿病心血管事件的机制。方法:用链脲佐菌素制作糖尿病大鼠模型,随机分为(1)糖尿病对照组,(2)糖尿病贝那普利干预组(10mg·kg^(-1)·day^(-1)),(3)糖尿病厄贝沙坦干预组(40mg·kg^(-1)·day^(-1)),(4)正常对照组。干预4周后用免疫组织化学方法对心脏组织PKCα、PKCβⅡ半定量测定,并进行对比分析。结果:与正常对照组相比,糖尿病组心脏PKCα、PKCβⅡ的表达增加。贝那普利,厄贝沙坦均能显著降低糖尿病心脏PKCα、PKCβⅡ的表达,且厄贝沙坦组PKCβⅡ表达比贝那普利降低更明显。结论:①PKC途径是糖尿病心血管并发症的机制之一;②抑制RAS减少糖尿病心血管事件可能与其调节PKC的表达有关。
Objective： To investigate the effects of blocking the rennin-angiotensin system on expression of protain kinase C isoforms in the heart of diabetic rats, investigate the machanisma of decreasing cardiovascular evants of diabetes by bloching RAS. Methods： Hyperglycemia was induced with streptozotocin and diabetic rats were randomized to 4 group ： normal control, diabetic control, benazepril group （ 10mg·kg^-1·day^-1 ）, irbesartan group （40mg·kg^-1·day^-1 ）. After 4 weeks, expression of PKCα、PKCβⅡ in the heart were assessed by immunohistochemistry. Resets： The expression of PKCα、PKCβⅡ was significantly highter in the heat of diabetic rats than that in normal ones. Treatment with benazepril, irbesartan partially corrected the abnormalities of expression, irbesartan decrease the expression of PKCβⅡ more than benazepril, Conclusion： （1）PKC pathway was one of mechanisms for cardiovascular eomplications of diabetes. （2）Decreasing cardiovascular evants of diabetes by bloching RAS perhaps associates with its effects on regulating PKC.
出处
《中国医药导刊》
2008年第2期261-263,共3页
Chinese Journal of Medicinal Guide
