青藤碱对急性心肌缺血再灌注损伤大鼠的保护作用  

Protective effect of sinomenine preconditioning on acute myocardial ischemiareperfusion injury in rats

作　　者：张风 郑刚(指导)[1] 齐婧[1,2] 徐佳萌 ZHANG Feng;ZHENG Gang;QI Jing;XU Jiameng(Shaanxi University of Chinese Medicine,Xianyang 712046,China)

机构地区：[1]陕西中医药大学,咸阳712046 [2]陕西中医药大学第二附属医院,咸阳712000

出　　处：《中国免疫学杂志》2022年第15期1833-1837,共5页Chinese Journal of Immunology

基　　金：陕西省重大病种中医药创新计划:胸痹(冠心病);陕西省中医管理局科研专项(15-SCJH015,15-SCJH016);陕西中医药大学第二附属医院学科创新团队专项(2020XKTD-B03)资助。

摘　　要：目的:本研究旨在探索青藤碱预处理对急性心肌缺血再灌注(I/R)损伤大鼠的保护作用及可能的机制。方法:将大鼠随机分为假手术(Sham)组,模型(I/R)组,青藤碱(SIN)组,维拉帕米(VP)组,结扎大鼠左冠状动脉前降支,制作急性心肌I/R损伤大鼠模型。再灌注2 h后监测各组大鼠心电图ST段变化,HE染色法观察心肌组织病理学变化,再灌注末抽取动脉血,ELISA测定乳酸脱氢酶(LDH)、肌酸激酶同工酶(CK-MB)、氨基末端脑钠肽前体(NT-proBNP)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、丙二醛(MDA)、TNF-α、IL-6含量。结果:VP组和SIN组可抑制急性心肌I/R损伤大鼠心电图ST段抬高,降低心肌酶LDH、CK-MB的活性和NT-proBNP的水平,可升高抗氧化应激因子SOD、CAT水平,降低促氧化因子MDA水平,可抑制炎症因子TNF-α、IL-6水平的升高,与I/R组相比差异均有统计学意义(P<0.05,P<0.01)。结论:SIN预处理可通过抑制氧化应激、炎症级联反应,对I/R大鼠产生保护作用。Objective:To explore the protective effect of sinomenine preconditioning on acute myocardial ischemia-reperfusion(I/R)injury in rats and its possible mechanism.Methods:Rats were randomly divided into sham operation(Sham)group,model(I/R)group,sinomenine(SIN)group,verapamil(VP)group,and ligation of the left anterior descending coronary artery of the rat to make rat model of acute myocardial I/R injury. After 2 hours of reperfusion,the ST segment changes of the rats in each group were monitored. The pathological changes of myocardial tissue were observed by HE staining. Arterial blood was drawn at the end of reperfusion. ELISA was used to determine lactate dehydrogenase(LDH)and creatine Kinase isoenzyme(CK-MB),N-terminal pro brain natriuretic peptide(NT-proBNP),superoxide dismutase(SOD),catalase(CAT),malondialdehyde(MDA),TNF-α,IL-6 contents.Results:VP group and SIN group could inhibit ST segment elevation,decrease the activities of myocardial enzymes LDH,CK-MB and NT-proBNP,increase the levels of antioxidant stress factors(SOD,CAT),decrease the levels of Pro-oxidant factors(MDA)and inhibit inflammatory factors(TNF-α,IL-6). Compared with I/R group,the differences were statistically significant(P<0.05,P<0.01).Conclusion:SIN preconditioning has protective effect on myocardial tissue of acute myocardial I/R rats,and can reduce the degree of heart failure in rats. The mechanism may be related to the inhibition of oxidative stress and inflammatory cascade.

关 键 词：青藤碱 心肌缺血再灌注 氧化应激 炎症反应 

分 类 号：R258.5[医药卫生—中医内科学]