Association between delayed cardioprotection of aged rat myocytes and activation of mitogen-activated protein kinase.
OBJECTIVE
To study the cardioprotective effects of hypoxic preconditioning (HPC) on aged rat ventricular myocytes and the cellular mechanism of protection.


METHODS
In the model of hypoxia/reoxygenation (H/R) of isolated ventricular myocytes of aged rat, the effects of HPC on aged rat ventricular myocytes against lethal H/R stimulated ischemia/reperfusion (I/R) injury 24 hours later and the changes of mitogen-activated protein kinase (MAPK) system were observed in the present study.


RESULTS
HPC attenuated the lactate dehydrogenase (LDH) release and ATP depletion in myocytes and increased the viability of myocytes. It was also found that MAPK and its down-stream kinase--S6 kinase were also activated after HPC.


CONCLUSIONS
There is delayed cardioprotection in cardiac myocytes of aged rat and the cellular mechanism underlying might involve the activation of MAPK system.
Liu
X
X
Institute of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853, China.
Wang
S
S
Wu
X
X
Tang
C
C
D000255:Adenosine Triphosphate / Q000032:analysis; D000375:Aging / Q000502:physiology*; D000818:Animals; D002478:Cells, Cultured; D004789:Enzyme Activation; D019157:Ischemic Preconditioning, Myocardial; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000502:physiology*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology; D051381:Rats; D017208:Rats, Wistar
D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; D020928:Mitogen-Activated Protein Kinases