首页 | 本学科首页   官方微博 | 高级检索  
     

内啡肽-1后处理对大鼠心肌缺血再灌注损伤的实验研究
引用本文:宗巧凤,程向阳,于影,张蔚屏,高琴,李正红. 内啡肽-1后处理对大鼠心肌缺血再灌注损伤的实验研究[J]. 金属学报, 2015, 20(2): 132-137
作者姓名:宗巧凤  程向阳  于影  张蔚屏  高琴  李正红
作者单位:1.蚌埠医学院生理学教研室,蚌埠 233000,安徽;2.蚌埠医学院第一附属医院麻醉科,蚌埠 233000,安徽
基金项目:安徽省教育厅自然科学研究重点项目(KJ2011A202);蚌埠医学院科技发展基金重点项目(Bykf13A10);蚌埠医学院研究生创新计划项目(Byycx1307)
摘    要:目的: 观察内啡肽-1(EM-1)后处理对大鼠心肌缺血再灌注损伤的影响。方法: 健康雄性SD大鼠48只,随机分为8组:假手术组(S组),缺血再灌组(IR组),缺血后处理组(IPO组),EM-1后处理10、20和 50 μg/kg(EM10、EM20、EM50)三组,EM-1 50 μg/kg+纳洛酮 3 mg/kg 后处理组(EM50+Nal组)、Nal后处理组(Nal组),均 i.v. 给药。结扎冠脉左前降支 30 min,再灌 120 min 造IR模型。全程监测心率(HR)、平均动脉压(MAP)和Ⅱ导联心电图(ECG)。动脉血浆检测丙二醛(MDA)含量及乳酸脱氢酶(LDH)和超氧化物歧化酶(SOD)的活性。结果: 除EM各组再灌注 120 min MAP外,IPO组和EM各组HR、MAP、RPP的下降程度均显著低于IR组(P<0.05,P<0.01);与IR组比较,IPO组和EM-1三个剂量组均使血浆LDH活性降低、MDA含量降低及SOD活性增加(P<0.05,P<0.01),且EM对MDA含量及SOD活性的影响呈剂量依赖;与EM50组比较,EM50+Nal组血浆LDH活性升高、MDA含量增加及SOD活性降低(P<0.05,P<0.01)。结论: EM-1后处理可能是通过激动阿片受体,引起MDA含量降低及SOD活性增加,发挥对心肌缺血再灌注损伤的保护作用。

关 键 词:内啡肽-1  阿片受体  心肌缺血再灌注  缺血后处理  心肌保护  
收稿时间:2014-07-11
修稿时间:2014-09-05

Experimental study of endomorphin-1 postconditioning against myocardial ischemia reperfusion injury in rats
ZONG Qiao-feng,CHENG Xiang-yang,YU Ying,ZHANG Wei-ping,GAO Qin,LI Zheng-hong. Experimental study of endomorphin-1 postconditioning against myocardial ischemia reperfusion injury in rats[J]. Acta Metallurgica Sinica, 2015, 20(2): 132-137
Authors:ZONG Qiao-feng  CHENG Xiang-yang  YU Ying  ZHANG Wei-ping  GAO Qin  LI Zheng-hong
Affiliation:1.Department of Physiology, Bengbu Medical College, Bengbu 233000, Anhui, China;2.Department of Anesthesiology,the First Affiliated Hospital of Bengbu Medical College, Bengbu 233000, Anhui, China
Abstract:AIM: To investigate the effects of endomorphin-1 (EM-1) postconditioning in rats on myocardial ischemia reperfusion injury.METHODS: 48 male Sprague Dawley rats were randomly divided into 8 groups:sham group (S group), ischemia-reperfusion group (IR group), ischemia postconditioning group (IPO group), EM-1 postconditioning groups (10, 20, 50 μg/kg) (EM10, EM20, EM50), EM-1 50 μg/kg+Naloxone 3 mg/kg postconditioning (EM50+Nal group), Naloxone postconditioning group (Nal group). The myocardial ischemia reperfusion injury model was established through occluding the left anterior descending branch of coronary artery for 30 min and reperfusing for 120 min in vivo. Heart rate (HR), mean arterial pressure (MAP), and Ⅱlead electrocardiogram were continuously monitored during the process. The arterial blood sample was obtained to measure plasma content of malondialdehyde(MDA) and the activities of lactate dehydrogenase (LDH), superoxide dismutase(SOD).RESULTS: In addition to the MAP of reperfusion 120 min in EM-1groups, the HR, MAP, RPP of IPO and EM-1 groups were significantly lower than IR group (P<0.05, P<0.01). Compared with IR group, the activity of LDH and content of MDA were decreased and the activity of SOD was increased (P<0.05,P<0.01) in IPO and EM-1 groups after reperfusion. EM-1 produced a dose-related effect on the content of MDA and the activity of SOD. The activity of LDH and content of MDA were higher and the activity of SOD was lower (P<0.01) in EM50+Nal group than in EM50 group after reperfusion.CONCLUSION: EM-1 postconditioning may produce the cardioprotection of myocardial ischemia reperfusion injury by activating opioid receptor, reducing the MDA and increasing the SOD.
Keywords:endomorphin-1  opioid receptor  myocardial ischemia reperfusion  ischemia postconditioning  cardioprotection  
点击此处可从《金属学报》浏览原始摘要信息
点击此处可从《金属学报》下载全文
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号