甘草查尔酮A对H_2O_2所致心肌细胞损伤的保护作用研究  

Protective effects of licorice chalcone A on cardiomyocyte injury induced by H_2O_2

作　　者：凌珅 吴梦玮[2] LING Shen;WU Meng-wei(Department of Orthopedics,Beijing No.1Integrated Chinese and Western Medicine Hospital,Beijing100025;Department of Physical Examination,Dongfang Hospital Affiliated to Beijing University of Traditional Chinese Medicine,Beijing100078)

机构地区：[1]北京市第一中西医结合医院骨伤科,北京100025 [2]北京中医药大学东方医院体检科,北京100078

出　　处：《世界中西医结合杂志》2018年第11期1544-1548,共5页World Journal of Integrated Traditional and Western Medicine

基　　金：北京中医药大学东方医院1166人才计划中青年专家基金

摘　　要：目的探讨甘草查尔酮A(LCA)对双氧水(H_2O_2)诱导的心肌细胞损伤的保护作用及其机制。方法将原代培养的乳鼠心肌细胞随机分为空白组、模型组(H_2O_2)、LCA低剂量组(10μmol/L)、LCA中剂量组(20μmol/L)、LCA高剂量组(40μmol/L)。经LCA给药4 h后,与100μM的H_2O_2共孵育24 h后检测细胞存活率,乳酸脱氢酶(LDH),脂质过氧化物丙二醛(MDA),活性氧自由基(ROS),Na+-K+-ATP酶,Ca^(2+)-ATP酶活性,同时检测过氧化物酶体增殖子活化受体γ(PPARγ),核因子E2相关因子2(Nrf2),和血红素加氧酶-1(HO-1) mRNA的表达情况。结果 LCA对H_2O_2所致心肌细胞损伤模型有保护作用,可抑制脂质过氧化MDA,ROS的生成,抑制Na+-K+-ATP酶活性,升高Ca^(2+)-ATP酶活性,上调PPARγ,Nrf2和HO-1 mRNA表达(P <0. 05,P <0. 01)。结论甘草查尔酮A对H_2O_2所致心肌细胞损伤有显著保护作用,且其作用机制可能与激活PPARγ/Nrf2/HO-1通路,缓解线粒体氧化应激有关。Objective To explore the protective effects of licorice chalcone A(LCA)on cardiomyocyte injury induced by hydrogen peroxide(H2O2)and its mechanism.Methods The primary cultured cardiomyocytes of the neonatal rats were randomized into a blank group,a model group(H2O2),a LCA low-dose group(10μmol/L),a LCA middle-dose group(20μumol/L)and a LCA high-dose group(40μmol/L).In4h after LCA medication and24h after co-incubation of H2O2100μM,the cell viability,LDH,MDA,ROS,Na^+-K^+-ATPase and Ca2^+-ATPase activity were detected,as well as the mRNA expressions of PPAR7,Nrf2and HO-1.Results LCA was protective to the model of cardiomyocyte injury induced by H2O2.It inhibited the production of MDA and ROS,inhibited Na^+-K^+-ATPase,increased Ca^2+-ATPase activity and up-regulated the mRNA expressions of PPAR7,Nif2and HO-1(P<0.05,P<0.01).Conclusion LCA presents the significant protection to cardiomyocyte injury induced by H2O2.The effect mechanism is probably related to the activation of PPARγ/NrfZ/HO-1passway and the relief of mitochondrial oxidative stress.

关 键 词：心肌细胞 甘草查尔酮A MDA LDH NA^+ -K^+ -ATP酶 PPARΓ Nrf2 

分 类 号：R285[医药卫生—中药学]