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| 激活κ-阿片受体抑制小鼠心肌缺血再灌注损伤的作用及研究 |
| Study on effect of Activation of κ-opioid Receptor Inhibiting Myocardial Ischemia Reperfusion Injury in Mice |
| 投稿时间：2019-06-01 修订日期：2019-06-01 |
| DOI： |
| 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） |
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| 中文摘要: |
| 目的： 探讨外源性κ-阿片受体激动剂 U50 488H对小鼠心肌缺血再灌注损伤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,收集血清检测血清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组心功能下调,心肌梗死面积、血清LDH和cTnI水平增加(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,血清LDH和cTnI水平减少(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的作用均被抑制。结论：κ-阿片受体激活可抑制心肌缺血再灌注损伤,改善心功能,该保护作用可能与抑制CaMKII磷酸化有关。 |
| 英文摘要: |
| 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 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 I/R group, U+I/R group showed improved cardiac function, decreased myocardial infarction area, the lever of LDH and cTnI in serum (P<0.05), and inhibited phosphorylated CaMKII in myocardial tissue (P<0.05). These effects of U50,488H were inhibited after the application of nor-BNI. Conclusion: κ-opioid receptor activation could inhibit myocardial ischemia-reperfusion injury and improve cardiac function, and the protective effect of κ-opioid receptor activation may be associated with the reduced expression level of p-CaMKII. |
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