益母草碱衍生物Ia通过激活蛋白激酶ε保护缺氧复氧心肌细胞  

Protective Effect of Leonurine Derivative Ia on Hypoxia/Reoxygenation Injury of Cardiomyocyte by Activating Protein Kinase Cε

作　　者：王锦芝[1] 王春燕[2] 盘鹰[1] 何小英[1] 

机构地区：[1]汕头大学医学院化学教研室,广东汕头515041 [2]香港大学李嘉诚医学院麻醉科,香港999077

出　　处：《汕头大学医学院学报》2015年第2期68-71,共4页Journal of Shantou University Medical College

基　　金：广东省医学科研基金资助项目(A2012380)

摘　　要：目的:观察益母草碱衍生物Ia对心肌细胞缺氧复氧(H/R)所致损伤的作用。方法:原代培养SD新生乳鼠心肌细胞,并制作H/R模型。Western blot检测蛋白激酶(PK)C转位;双抗体夹心光化学法和ELISA分别测定肌钙蛋白(c Tn)I浓度和肿瘤坏死因子(TNF)-α;观察心肌细胞损伤状况及内皮细胞H/R后与血小板间的相互作用。结果:心肌细胞H/R时,PKCε激活并转位;益母草碱衍生物Ia可促使PKCε激活和转位,并减少肌酸激酶、c Tn I漏出和TNF-α分泌。结论:益母草衍生物Ia对培养心肌细胞H/R损伤有保护作用,可能与其激活PKCε转位相关。Objective：To observe the protective effect of leonurine derivative Ia on hypoxia/reoxygenation（H/R）injury of cardiomyocyte. Methods：Neonatal rats cardiomyocytes were primarily cultured and the H/R model was prepared. The protein kinase（PK）C translocation was determined by Western blot. The cardiac troponin（c Tn）I release was determined by double antibody sandwich photochemical method and the tumor necrosis factor（TNF）-α was determined by ELISA to assess the degree of injury of cardiomyocytes. Results：When H/R in cardiomyocytes,PKCε was significantly activated. The leonurine derivative Ia could increase the translocation,and reduce the levels of creatine kinase,c Tn I and TNF-α. Conclusion：The myocardial protection of leonurine derivative Ia can depend on PKCε activation.

关 键 词：益母草碱衍生物 缺氧复氧 蛋白激酶C 合成 

分 类 号：R966[医药卫生—药理学]