Morphine preconditioning confers cardioprotection in doxorubicin-induced failing rat hearts via ERK/GSK-3β pathway independent of PI3K/Akt.
作者： Shu-Fang He , Shi-Yun Jin , Hao Wu , Bin Wang , Yun-Xiang Wu
DOI: 10.1016/J.TAAP.2015.08.007
关键词:
摘要: Preconditioning against myocardial ischemia-reperfusion (I/R) injury can be suppressed in some pathological conditions. This study was designed to investigate whether morphine preconditioning (MPC) exerts cardioprotection doxorubicin (DOX)-induced heart failure rats and the mechanisms involved. Phosphatidylinositol-3 kinase/protein kinase B (PI3K/Akt), extracellular signal-regulated (ERK) glycogen synthase (GSK)-3β pathways were examined. Normal DOX-induced failing rat hearts subjected I/R using a Langendorff perfusion system with or without MPC ischemic (IPC). The PI3K inhibitor (wortmannin) ERK (PD98059) infused before MPC. In normal hearts, both IPC significantly reduced infarct size rise lactate dehydrogenase (LDH) level caused by injury. Pretreatment wortmannin PD98059 abrogated protective effects of phosphorylation Akt, GSK-3β. however, retained its while did not. effect abolished but not wortmannin. increased p-ERK rather than p-Akt. GSK-3β induced reversed only. elevate expression p-ERK, p-Akt p-GSK-3β hearts. We conclude that is cardioprotective appears mediated via ERK/GSK-3β pathway independent PI3K/Akt.
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