• Jia-ping Zhang, Yue-sheng Huang, and Zong-cheng Yang.
• State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Burns, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
• Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2005 Mar 1; 17 (3): 150-3.

ObjectiveTo observe the activation and explore the role of three major mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase (ERK), p38 kinase and c-Jun NH(2)-terminal protein kinase (JNK), in cardiomyocytes injury induced by serum after hypoxia and burn injury.MethodsPhosphorylation of the three major MAPKs in primary cultured neonatal rat cardiomyocytes were determined by Western blotting. Contents of released lactate dehydrogenases (LDH) and death-rate of myocytes treated with serum after hypoxia and burn injury, SB203580+hypoxia and burn serum, PD98059+hypoxia and burn serum were observed respectively.ResultsExposing rat neonatal cardiomyocytes to hypoxia and burn serum resulted in a rapid and prolonged activation of p38 kinase and ERK. Phosphorylation degree of p38 kinase, ERK1/2 was increased. Myocytes treated with SB203580 (10 micromol/L), a selective inhibitor of p38 kinase, resulted in a significant decline in LDH leakage leaking and cell death. However, with pretreatment of cell with PD98059(25 micromol/L), an inhibitor of ERK, LDH leakage and cell death were increased.ConclusionSerum obtained after hypoxia and burn injury activate p38 kinase and ERK, but not JNK, in cardiomyocytes. p38 kinase pathway might play a role in mediating cardiomyocytes injury, whereas ERK plays a protective role.

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