脑钠肽后处理对大鼠缺血再灌注损伤心肌细胞凋亡的保护作用与机制研究  

Protective effect of brain natriuretic peptide postconditioning on cardiomyocyte apoptosis induced by myocardial ischemia reperfusion injury in rats and a study on mechanism

作　　者：董小莉[1] 谭宁[2] 马立宁[1] 王苗[1] 李斌[1] 王圣[1] 邓宇珺[2] 符永恒[2] Dong Xiaoli;Tan Ning;Ma Lining;Wang Miao;Li Bin;Wang Sheng;Deng Yujun;Fu Yongheng(People's Hospital of Hainan Province,Haikou 570311,China;不详)

机构地区：[1]海南省人民医院海南医学院附属海南医院心血管内科,海南省临床医学研究院,海南省医学院临床学院,海口570311 [2]广东省医学科学院,广东省人民医院心血管内科,广东省心血管病研究所,广州510080

出　　处：《中国循证心血管医学杂志》2020年第9期1087-1090,共4页Chinese Journal of Evidence-Based Cardiovascular Medicine

基　　金：广东省自然科学基金资助项目(9121008002000002);海南省自然科学基金资助项目(818MS132)。

摘　　要：目的探讨脑钠肽(BNP)对心肌缺血再灌注损伤时心肌细胞凋亡的保护作用及其机制。方法将24只SD大鼠随机分入假手术组(S组)、缺血再灌注组(I/R组)、BNP组、BNP+2-巯基丙酰甘氨酸组(BNP+MPG组),结扎前降支,缺血35 min,再灌注120 min制作心肌缺血再灌注模型。其中S组只在前降支下穿针过线,不结扎前降支。各组均于前降支过线/结扎后10 min开始尾静脉恒速泵入相应药物直至再灌注结束。S组泵入生理盐水,I/R组泵入生理盐水、BNP组泵入BNP[0.01 g/(kg·min)];BNP+MPG组泵入BNP[0.01 g/(kg.min)]并在缺血25 min后经尾静脉弹丸注射MPG(20 mg/kg);再灌注结束后取心脏,检测心肌超氧化物歧化酶(SOD)、硫代巴比妥酸法测定丙二醛(MDA)含量及心肌细胞凋亡率。结果与I/R组相比较,BNP组的SOD活性显著升高,MDA含量显著下降,心肌细胞凋亡率明显下降,提示BNP可以降低氧化应激水平并因此对缺血再灌注损伤的产生保护作用;与BNP组相比较,BNP+MPG组SOD活性显著降低,MDA含量显著增加,心肌细胞凋亡率明显升高,提示BNP对可能通过控制活性氧(ROS)水平对缺血再灌注心肌细胞产生保护作用。提示BNP对缺血再灌注心肌的保护作用与ROS有关。结论BNP降低缺血再灌注心肌细胞凋亡的作用与ROS有关。Objective To discuss the protective effect of brain natriuretic peptide(BNP)on cardiomyocyte apoptosis induced by myocardial ischemia reperfusion injury(MIRI)and investigate the mechanism.Methods SD rats(n=24)were divided into sham-operation group(S group),ischemia reperfusion group(I/R group),BNP group and BNP+MPG group.MIRI model was established by ligation of anterior descending branch of coronary artery induced ischemia for 35 min and reperfusion for 120 min,while S group was only given a sham-operation.After the ligation for 10 min corresponding medicines were pumped into caudal vein in a constant speed in all groups.S group and I/R group were given normal saline,BNP group was given BNP[0.01 g/(kg·min)],BNP+MPG group was given BNP[0.01 g/(kg·min)]and after ischemia for 25 min was given MPG(20 mg/kg).The cardiac samples were collected at the end of reperfusion.The activity of superoxide dismutase(SOD)was detected by using XTO method,and level of malondialdehyde(MDA)and myocardial apoptosis rate were detected by using thiobarbituric acid method.Results SOD activity increased significantly and MDA level and cardiomyocyte apoptosis rate decreased significantly in BNP group compared with I/R group,which indicated that BNP reduced oxidative stress level and had a preventive effect on MIRI.SOD activity decreased significantly and MDA level and cardiomyocyte apoptosis rate increased significantly in BNP+MPG group compared with BNP group,which indicated that BNP prevented MIRI possibly through controlling level of reactive oxygen species(ROS).The protective effect of BNP on I/R myocardium was correlated to ROS.Conclusion BNP can reduce I/R cardiomyocyte apoptosis rate,which is correlated to ROS.

关 键 词：脑钠肽 活性氧 氧化应激 心肌缺血再灌注损伤 心肌细胞凋亡 大鼠 

分 类 号：R541.4[医药卫生—心血管疾病]