| 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].,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 |
| 投稿时间：2019-06-01 修订日期：2019-06-25 |
| 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） |
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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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