Objective: To investigate the cardioprotective effect of mitogen-activated protein kinases (MAPKs) of ischemic preconditioning (IPC) in rat heart.
Methods: In the model of ischemia/reperfusion (I/R) of isolated perfused SD rat heart, the effect of IPC on I/R injury was observed. The activities of MAPK family members, ERKs, p38 and SAPK, and their relationship with IPC phenomenon were also observed.
Results: IPC significantly improved myocardial functions in heart subjected to I/R injury, and attenuated leakage of myocardial creatine kinase and depletion of ATP. IPC activated ERK and p38 kinase. Their activities were increaed by 73% (P < 0.01) and 69% (P < 0.01) respectively. However, IPC showed no effect on myocardial SAPK activity. Preparation with genistein (an inhibitor of tyrosine kinase) and PD098059 (an inhibitor of ERK) abolished IPC cardioprotection, while p38 kinase inhibitor SB202190 had no effect on IPC.
Conclusions: ERKs, but not p38 and SAPK of MAPK, mediates the IPC cardioprotective effect.