Article Summary
武敏1 郭海涛2 时全星2 李娟2 师建国1△ 裴建明2.第四军医大学基础部病理学教研室[J].现代生物医学进展英文版,2011,11(20):3809-3815.
第四军医大学基础部病理学教研室
Endogenous Kopioid Peptide Mediated Ischemic Postconditioning forCardioprotectiong
  
DOI:
中文关键词: 后处理  凋亡  心脏  κ- 阿片受体  强啡肽
英文关键词: Postconditioning  Apoptosis  Heart  κopioid receptor  Dynorphin
基金项目:国家自然科学基金(30971060,30900535),国家重大新药项目基金(2009ZX09301-009-BD10)
Author NameAffiliation
WU Min1,GUO Hai-tao2, SHI Quan-xing2, LI Juan2 , SHI Jian-guo1△, PEI Jian-ming2 第四军医大学基础部病理学教研室 
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中文摘要:
      目的:研究内源性κ- 阿片受体(κ-OR)的激动剂强啡肽在触发缺血后处理(postconditioning,Postcon)中的抗凋亡作用及潜 在机制。方法:除了假手术组,SD 大鼠(每组6 只)制作缺血再灌注模型,进行了左冠状动脉前降支闭合30 分钟后,再灌注2 小时 伴有或不伴有缺血后处理。在再灌注前5 分钟静脉注射选择性κ- 受体拮抗剂nor-binaltorphimine(nor-BNI)。氯化三苯四染色测 定心肌梗死面积。用分光光度计测定血浆中肌酸激酶(CK)、乳酸脱氢酶(LDH)水平和心肌细胞凋亡蛋白酶-3(caspase-3)活性。 TUNEL 法检测心肌细胞凋亡。ELISA 法检测血清和心肌中强啡肽含量。结果:缺血/ 再灌注(I/R 组)组的梗死面积,caspase-3 活 性,细胞凋亡指数,CK 和LDH 活性等明显高于假手术组(P<0.01)。与I/R 组相比,Postcon 明显减少梗死面积,caspase-3 活性,细 胞凋亡指数,CK 及LDH 活性(P<0.01)。Postcon 可使强啡肽含量显著增加(P<0.01)。除强啡肽含量外,上述所有的作用均被 nor-BNI 所阻断。结论:心脏保护和后处理的抗凋亡作用是通过激活κ-OR,至少部分通过增加强啡肽的水平来介导的。
英文摘要:
      Objective: To investigate the mechanism of dynorphin, an endogenous kappa opioid receptor (κ-OR) agonist in postconditioning (Postcon). Methods: Sprague Dawley (SD) rats (n=6) underwent a 30-min left anterior descending occlusion followed by 2h of reperfusion with or without a Postcon stimulus. The selective κ-OR antagonist nor-binaltorphimine (Nor-BNI) was administered i.v. 5 min before reperfusion. Infarct size was determined by triphenyltetrazolium chloride staining. Blood plasma of creatine kinase (CK) and lactate dehydrogenase (LDH) and myocardial caspase-3 activity were analyzed by spectrophotometrically. Myocardial apoptosis was analyzed by detection of TUNEL. Immunoreactive dynorphin in blood serum and myocardium was measured by an antigen-competitive ELISA. Results: Infarction size, caspase-3 activity, apoptotic index, CK and LDH were significantly higher in ischemic/reperfusion (I/R) group than that in vehicle group (P<0.01). Postcon reduced infarction size, caspase-3 activity, apoptotic index, CK and LDH (P<0.01 vs. I/R). Dynorphin content significantly increased after Postcon (P<0.01). All indexes described above were abolished by Nor-BNI, with the exception of dynorphin content. Conclusion: Cardiac protection and anti-apoptotic effect of Postcon is mediated by activation ofκ-OR. Effect of Postcon is mediated, at least partially, by enhanced dynorphin expression.
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