[The role of mitogen-activated protein kinases family in ischemic preconditioning of rat heart].
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.
Liu
X
X
Institute of Geriatric Cardiology, PLA General Hospital, Beijing 100853.
Yang
J
J
Wang
S
S
D000818:Animals; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D048051:p38 Mitogen-Activated Protein Kinases
D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases