Article Summary
王凯燕,刘振华,王渊博,史 睿,刘超阳,付 峰,李 娟,张淑苗,郭海涛,裴建明.激活κ-阿片受体抑制小鼠心肌缺血再灌注损伤的作用及机制[J].现代生物医学进展英文版,2019,19(24):4624-4627.
激活κ-阿片受体抑制小鼠心肌缺血再灌注损伤的作用及机制
Role of Activation of κ-opioid Receptor in Inhibiting Myocardial Ischemia Reperfusion Injury in Mice
Received:June 01, 2019  Revised:June 25, 2019
DOI:10.13241/j.cnki.pmb.2019.24.005
中文关键词: 心肌缺血再灌注损伤  κ-阿片受体  钙/钙调蛋白依赖的蛋白激酶Ⅱ
英文关键词: Myocardial ischemia reperfusion injury  κ-opioid receptor  CaMKII
基金项目:国家自然科学基金项目(81770243);陕西省中药管理局中医药项目(JCMS058);陕西省自然科学基础研究计划(2018JM7114)
Author NameAffiliationE-mail
WANG Kai-yan Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China wgkaiyan@163.com 
LIU Zhen-hua Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China  
WANG Yuan-bo Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China  
SHI Rui Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China  
LIU Chao-yang Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China  
FU Feng Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China  
LI Juan Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China  
ZHANG Shu-miao Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China  
GUO Hai-tao Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China  
PEI Jian-ming Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China  
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中文摘要:
      摘要 目的:探讨外源性κ-阿片受体激动剂 U50,488H对小鼠缺血再灌注损伤心肌的保护作用及其机制。方法:选择成年雄性C57小鼠40只,将其随机分为4组:假手术组(Sham),缺血再灌注组(I/R),κ-阿片受体激动剂 U50,488H+I/R组(U+I/R),κ-阿片受体阻断剂nor-BNI+U50,488H+I/R组(N+U+I/R)。建立小鼠急性心肌缺血再灌注在体模型,通过小动物超声仪检测小鼠心功能,采用氯化三苯基四氮唑-伊文思蓝双染检测心肌梗死面积,检测血清心肌损伤物LDH活性和cTnI含量,Western-Blot检测Ca MKII和磷酸化Ca MKII的表达。结果:与Sham组相比,I/R组小鼠心功能下降,心肌梗死面积增加,血清LDH和cTnI水平升高(P<0.05),心肌组织内磷酸化Ca MKII的表达明显增加(P<0.05);与I/R组相比,U+I/R组心功能改善,心肌梗死面积减小,血清LDH和cTnI水平降低(P<0.05),心肌组织内CaMKII磷酸化被抑制(P<0.05)。给予nor-BNI后,上述U50,488H的作用均被阻断。结论:κ-阿片受体激活可抑制CaMKII磷酸化并抑制心肌缺血再灌注损伤,改善心功能。
英文摘要:
      ABSTRACT Objective: To investigate the protective effect of exogenous κ-opioid receptor agonist U50,488H on myocardial ischemia reperfusion injury in mice and its potential underlying mechanism. Methods: 40 adult male C57 mice were randomly divided into 4 groups: Sham group (Sham), ischemia-reperfusion group (I/R), κ-opioid receptor agonist U50,488H+I/R group (U+I/R), κ-opioid receptor blocker nor-BNI+U50,488H+MI/R group (N+U+I/R). In vivo model of acute myocardial ischemia reperfusion in mice was established. The cardiac function was detected by ultrasound of small animals. Myocardial infarction area was detected by TTC/Evean's blue staining. Serum LDH activity and cTnI content were collected and detected by kits. The expression of CaMKII and phosphorylated CaMKII were detected by western-blotting. Results: Compared with the sham group, cardiac function was decreased in I/R group, myocardial infarction area and the lever of serum LDH and cTnI were increased in serum(P<0.05), and the expression of phosphorylated CaMKII in myocardial tissue was significantly increased (P<0.05). Compared with the I/R group, the U+I/R group showed improved cardiac function, decreased myocardial infarction area, the decreased levels of LDH and cTnI in the serum (P<0.05), and inhibited phosphorylated CaMKII in the myocardial tissue(P<0.05). These effects of U50,488H were blocked by nor-BNI. Conclusion: κ-opioid receptor activation inhibits myocardial ischemia-reperfusion injury and improves cardiac function, and the protective effect of κ-opioid receptor activation may be associated with the reduced expression level of p-CaMKII, which needs further investigation.
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