阿托伐他汀对急性心肌梗死动物模型Nrf2/HO-1途径的影响  

Influence of atorvastatin on Nrf2/HO-1 pathway in animal model of acute myocardial infarction

作　　者：王志利 刘锋[2] 赵晓燕[3] Wang Zhili;Liu Feng;Zhao Xiaoyan(Department of Cardiology,People's Hospital of Linzhou City,Henan Province,Linzhou 456550,China;不详)

机构地区：[1]林州市人民医院心内科,林州456550 [2]郑州大学第一附属医院彩超中心,郑州450000 [3]郑州大学第一附属医院心内科,郑州450000

出　　处：《中国循证心血管医学杂志》2020年第8期971-974,共4页Chinese Journal of Evidence-Based Cardiovascular Medicine

摘　　要：目的探究阿托伐他汀(ATV)对急性心肌梗死(AMI)动物模型Nrf2/HO-1途径的影响。方法30只大鼠随机分为Sham组、AMI组和AMI+ATV组3组(每组各10只)。AMI组和AMI+ATV组大鼠通过结扎建立AMI模型,AMI+ATV组大鼠使用ATV灌胃(10 mg/kg,1/d,7 d)。比较各组大鼠的心功能、梗死面积、心肌细胞凋亡、血清氧化应激和炎性因子、梗死边缘组织中Nrf2/HO-1水平。结果与Sham组比较,AMI组的左室收缩末期压力(LVESP)、±dP/dt max、超氧化物歧化酶(SOD)及Nrf2/HO-1水平降低(P<0.05);左室舒张末期压力(LVEDP)、梗死面积、凋亡指数、血清白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、丙二醛(MDA)升高(P<0.05)。AMI+ATV组的LVESP、±dP/dt max、SOD及Nrf2/HO-1水平显著高于AMI组(P<0.05);而LVEDP、梗死面积、凋亡指数、IL-6、TNF-α、MDA显著低于AMI组(P<0.05)。结论ATV可能通过促进Nrf2/HO-1通路抑制以抑制氧化应激和炎性反应,从而减少AMI模型大鼠的心肌细胞凋亡,保护心功能。Objective To discuss the influence of atorvastatin(ATV)on Nrf2/HO-1 pathway in animal model of acute myocardial infarction(AMI).Methods SD rats(n=30)were divided randomly into Sham group,AMI group and AMI+ATV group(each n=10).The model of AMI was established through ligation in AMI group and AMI+ATV group,and AMI+ATV group was orally given ATV(10 mg/kg,1/d,7 d).The heart function,infarction size,cardiomyocyte apoptosis,serum oxidative stress factors and inflammatory factors,and level of Nrf2/HO-1 in infarction marginal tissue were compared among 3 groups.Results Compared with Sham group,the levels of left ventricular end-systolic pressure(LVESP),±dP/dt max,superoxide dismutase(SOD)and Nrf2/HO-1 decreased(P<0.05),and levels of left ventricular end-diastolic pressure(LVEDP),infarction size,apoptosis index,serum interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)and malondialdehyde(MDA)increased(P<0.05)in AMI group.The levels of LVESP,±dP/dt max,SOD and Nrf2/HO-1 were significantly higher in AMI+ATV group than those in AMI group(P<0.05).The levels of LVEDP,infarction size,apoptosis index,IL-6,TNF-αand MDA were significantly lower in AMI+ATV group than those in AMI group(P<0.05).Conclusion ATV can inhibit oxidative stress and inflammatory response,relieve cardiomyocyte apoptosis and protect heart function possibly through improving the inhibition of Nrf2/HO-1 pathway in AMI rat model.

关 键 词：急性心肌梗死 阿托伐他汀 凋亡 Nrf2/HO-1 氧化应激 大鼠 

分 类 号：R542.22[医药卫生—心血管疾病]