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Updated: Jun 27, 2026

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
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Role of p38 mitogen-activated protein kinases in cardioprotection of morphine preconditioning

Ye Zhang1, Er-wei Gu, Jian Zhang

  • 1Department of Anesthesiology, First Affiliated Hospital of Anhui Medical University, Hefei 230022, China. zhangye@mail.hf.ah.cn

Chinese Medical Journal
|May 29, 2007
PubMed
Abstract

Insights

Morphine-induced preconditioning (MPC) and ischemic preconditioning (IPC) protect rat hearts from injury. p38 mitogen-activated protein kinases (MAPK) mediate MPC, but trigger and mediate IPC.

Area of Science:

  • Cardiovascular Science
  • Molecular Cardiology
  • Pharmacology

Background:

  • p38 mitogen-activated protein kinases (MAPK) are crucial for cardioprotection during ischemic preconditioning (IPC).
  • The role of p38 MAPK in morphine-induced preconditioning (MPC) remains unclear.

Purpose of the Study:

  • To investigate whether p38 MAPK activation mediates the protective effects of MPC against myocardial ischemia-reperfusion injury in a rat model.
  • To compare the role of p38 MAPK in MPC versus IPC.

Main Methods:

  • Male Spargue-Dawley rats were subjected to control, p38 MAPK inhibition (SB 203580), MPC, IPC, or combinations thereof.
  • Infarct size (IS) as a percentage of area at risk (AAR) was determined using triphenyltetrazolium staining.
  • p38 MAPK protein expression was assessed via Western blotting.

Main Results:

  • Both IPC and MPC significantly reduced infarct size compared to control.
  • Inhibition of p38 MAPK abolished the protective effect of IPC but not MPC when administered before preconditioning.
  • Inhibition of p38 MAPK prior to sustained ischemia diminished the protective effects of both MPC and IPC.
  • Phospho-p38 MAPK levels increased rapidly during ischemia and reperfusion in IPC, but only during reperfusion in MPC.

Conclusions:

  • p38 MAPK acts as a mediator in MPC.
  • p38 MAPK functions as both a trigger and a mediator in IPC.
  • These findings differentiate the mechanistic roles of p38 MAPK in two distinct preconditioning paradigms.

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