贝那普利阻断RAS系统对自发性高血压大鼠心肌JAK-STAT信号通路的影响  

The influence of benazepril blocking RAS on JAK-STAT signal transduction pathway of SHR′s myocardium

作　　者：刘雪平[1] 董泗芹[1] 郑敏[1] 张子强[2] 邵建华[3] 

机构地区：[1]山东大学山东省立医院保健科,山东济南250021 [2]千佛山医院ICU [3]山东省立医院保健心内科

出　　处：《中国老年学杂志》2007年第17期1651-1654,共4页Chinese Journal of Gerontology

基　　金：中央保健专项资助课题(鲁A032)

摘　　要：目的探讨贝那普利对自发性高血压大鼠(SHR)心肌组织JAK-STAT信号转导通路及细胞凋亡的影响。方法30周龄WKY大鼠12只,同龄SHR24只,随机分为SHR组,贝那普利组10mg/(kg·d)。RT-PCR法检测AT1mRNA、AT2mRNA表达,免疫组化法检测心肌组织STAT1、STAT3表达及TUNEL末端标记法进行细胞凋亡检测。结果与SHR组比较,贝那普利组AT1mRNA表达水平显著降低(P<0.01),AT2mRNA表达水平显著增高(P<0.01)。与SHR组比较,贝那普利能降低STAT1表达(P<0.01),升高STAT3表达(P<0.01)。贝那普利组心肌细胞凋亡显著低于SHR组(P<0.01)。结论贝那普利能调节心肌组织JAK-STAT信号转导通路,抑制细胞凋亡,从而发挥其心脏保护作用。　Objective To investigate the effects of benazepril on regulating JAK-STAT signal pathway and apoptosis of spontaneous hypertensive rat （SHR）＇s myocardium.Methods 12 Wistar-Kyoto （WKY） rats and 24 SHRs aged 30 weeks selected were randomly divided into SHR group and benazepril group （10 mg·kg^-1·d^-1）. The mRNA expression levels of AT1 and AT2 were detected by RT-PCR; the STAT1, STAT3 expression level of the myocardium was determined by immunohistochemical methods; apoptosis rate of myocardial cells was measured by TUNEL end-labelling.Results AT1 mRNA and STAT1 in protein expression of benazepril group was significantly lower than those of SHR group（P〈0.01）, AT2 mRNA and STAT3 in protein expression of benazepril group was significantly higher than that of SHR group（P〈0.01）. The apoptosis rate of SHR group was significantly higher than that of benazepril group（P〈0.01）.Conclusions Benazepril can regulate the SHR′s JAK-STAT signal transduction pathway of myocardium, inhibit apoptosis of myocardium to educe protective effect on the heart.

关 键 词：贝那普利 JAK-STAT 肾素-血管紧张素系统 细胞凋亡 

分 类 号：R544.1[医药卫生—心血管疾病]