ERK1/2与p38信号通路介导三七皂苷R1抗H_2O_2致心肌细胞损伤作用  

Notoginsenoside R1 Alleviates Cardiomyocytes Injury Induced By H_2O_2 Through ERK1/2 And p38 Signal Pathway

作　　者：周凤华[1] 潘芸芸[1] 崔小冰[2] 贾钰华[1] 

机构地区：[1]南方医科大学中医药学院,广州510515 [2]南方医科大学中西医结合医院,广州510310

出　　处：《中药药理与临床》2016年第2期17-20,共4页Pharmacology and Clinics of Chinese Materia Medica

基　　金：国家自然科学基金(No.81373574;81403339);广东省自然科学基金博士启动项目(No.2014A030310150);广东省中医药管理局科研项目(No.20141186);广州市海珠区科技计划项目(No.2013-cg-35);南方医科大学科研启动计划(No.PY2013N014)

摘　　要：目的:研究三七皂苷R1对过氧化氢(H2O2)诱导乳鼠心肌细胞损伤的影响及对细胞外调节蛋白激酶1/2(extracellular regulated protein kinase,ERK1/2)与p38通路的调节。方法:以50μmol/L H2O2干预原代培养心肌细胞3 h建立氧化损伤模型,分别观察0.1、1、10μmol/L三七皂苷R1对细胞活力、凋亡及细胞内过氧化物酶LDH、MDA及SOD的表达情况,再检测p-ERK1/2及p-p38蛋白水平;分别以ERK1/2与p38通路特异性阻断剂干预细胞,观察两者对心肌细胞的影响。结果:三七皂苷R1显著增加细胞活力,抑制细胞凋亡,降低LDH与MDA浓度,增加SOD活性,并且能明显降低p-ERK1/2与p-p38表达,以10μmol/L三七皂苷R1干预效果最明显(P<0.01)。阻断ERK1/2与p38通路后,细胞活力增加,凋亡率降低,LDH与MDA浓度降低,SOD活性明显增加。结论:三七皂苷R1能显著减轻H2O2诱导心肌细胞损伤,增加细胞活力,降低凋亡率,主要与调节ERK1/2及p38信号通路有关。Objective： To study the effect of Notoginsenoside R1 on the cardiomyocyte injury induced by H2O2. Methods： The primary cultured cardiomyocytes were incubated by H2O2 to establish cellular injury model; Cardiomyocytes were incubated with Notoginsenoside R1 at the concentrations of 0. 1,1 and 10 μmol / L,respectively. MTT was used to detect the cell viability and flow cytometry for apoptosis. The concentration of LDH,MDA and SOD were determined according to the kit instruction. The expression of p-ERK1 /2,p-p38,ERK1 /2 and p38 were detected by western blotting. Results： Notoginsenoside R1 significantly not only increased the cell activity,but also inhibited cell apoptosis,mainly through down-regulating the concentration of LDH and MDA,up-regulating SOD activity. It could also significantly decreased pp38 and p- ERK1 /2 expression,especially at the concentration of 10 μmol / L of Notoginsenoside R1. The difference between the H2O2 group and Notoginsenoside R1 group was statistically significant（ P 〈 0. 01）. After blocking ERK1 /2 and p38 pathway,cell viability increased,apoptosis rate decreased,the concentrations of LDH and MDA decreased,SOD activity increased,and the difference was statistically significant compared with those in H2O2group（ P 〈 0. 01）. Conclusion： Notoginsenoside R1 can alleviates cardiomyocyte injury induced by H2O2,mainly through inactivating ERK1 /2 and p38 signal pathway.

关 键 词：三七皂苷R1 心肌细胞 细胞外调节蛋白激酶1/2 P38 氧化应激 

分 类 号：R285[医药卫生—中药学]