文章基本信息
- 标题：Kappa-opioid receptor activation during reperfusion limits myocardial infarction via ERK1/2 activation in isolated rat hearts
- 本地全文：下载
- 作者：Kim, June Hong ; Jang, Young Ho ; Chun, Kook Jin 等
- 期刊名称：Korean Journal of Anesthesiology
- 印刷版ISSN：2005-6419
- 出版年度：2011
- 卷号：60
- 期号：5
- 页码：351-356
- DOI：10.4097/kjae.2011.60.5.351
- 语种：English
- 出版社：The Korean Society of Anesthesiologists,
- 摘要：Background
We investigated whether p42/p44 extracellular signal-regulated kinases (ERK1/2) and/or phosphatidylinositol-3-OH kinase (PI3K)-Akt play a crucial role in cardioprotection by κ-opioid receptor (KOP) activation.
MethodsLangendorff perfused rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Antagonists of ERK1/2 and PI3K were perfused in hearts treated with the KOP agonist U50488H (U50). Infarct size was measured after 2 h of reperfusion. The phosphorylation states of ERK1/2 and Akt by Western immunoblots were determined. Drugs were perfused for a period of 5 min before and 30 min after reperfusion.
ResultsInhibition of ERK1/2 (26.8 ± 2.9%, P < 0.05 vs. U50) but not PI3K (15.5 ± 1.1%, P > 0.05 vs. U50) completely abrogated the anti-infarct effect of U50488H. Western blot analysis revealed a significant increase in ERK1/2 but not Akt phsophorylation in U50488H-treated hearts as compared to control hearts when measured immediately after reperfusion.
ConclusionsKOP activation effectively reduces myocardial infarction. The anti-infarct effect of U50488H is mediated by the ERK1/2, but not the PI3K-Akt pathway.
- 关键词：Coronary occlusion; heart; Myocardial function; Opioid receptors; reperfusion
