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Different of ERK_(1/2) and p38 MAPK_(#alpha#/#beta#) in cellular signaling during cardiomyocyte anoxia preconditioning

Huang Yifeng, Gong Kaizheng, Zhang Zhengang

Department of Cardiology,The 2nd Clinical Medical College of Yangzhou University.Yangzhou 225001,Jiangsu

Abstract

The results obtained are as follows: (1) PD98059 (but not SB203580), administered in preconditioning anoxia phase in APC group, abolished completely the delayed protection of APC; (2) SB203580 administered in sustained anoxia phase in A/R group could relieve cell injury induced by anoxia, but not by PD98059; (3) the highest activity of ERK_(1/2) and p38 MAPK induced by anoxia appeared at 4h after the beginning of sustained anoxia. APC inhibited the over activation of both ERK_(1/2) and p38 during the following sustained anoxia. These results suggest that ERK_(1/2) activation during preconditioning may be an important link of cell signal signal transduction in the mechanism of APC delayed protection. p38_(#alpha#/#beta#) activation at the preconditioning stage dose not participate in signaling of APC delayed protection. The excessive activation of p38_(#alpha#/#beta#) is possibly a key factor in mediating cell injury induced by sustained anoxia. The inhibition of p38_(#alpha#/#beta#) excessive activation during subsequent sustained anoxia might play a role in delayed protection mechanism of APC.

Key words: Physiology;Cytoprotection anoxia;Ischemic;Preconditioning myocardial;Extracellular signal-regulated kinase p38;Mitogen-activated protein;Kinases

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Citing This Article：

Huang Yifeng, Gong Kaizheng, Zhang Zhengang. Different of ERK_(1/2) and p38 MAPK_(#alpha#/#beta#) in cellular signaling during cardiomyocyte anoxia preconditioning. Acta Physiol Sin 2003; 55 (4): (in Chinese with English abstract).