作者: Deepa S Nagarkatti , I Sha Ramadan
关键词: Protein kinase C 、 ASK1 、 Mitogen-activated protein kinase kinase 、 MAP kinase kinase kinase 、 Biology 、 Molecular biology 、 Protein kinase B 、 Protein kinase R 、 Cyclin-dependent kinase 2 、 Cell biology 、 MAPK14 、 Cardiology and Cardiovascular Medicine
摘要: Abstract The current study focuses on the role of p38 MAP kinase in response to acute preconditioning stimuli and ischemia. Exposure rat myoblast cell line H9C2 stimuli, viz. brief duration ischemia (metabolic inhibition) adenosine, led activation kinase. protective effect these against lethal ischemic insult was abolished presence inhibitor SB 203580 but not MEK PD 98509. Phorbol myristate acetate, PMA, which activates protein C, PKC, kinase, this is inhibited by PKC Go6850. PMA also C This indicates that action mediated via Paradoxically, Go6850 during stress protected cells death. mode death whether necrotic or apoptotic has been established. Lethal Preconditioning decreases second stress. These findings highlight preconditioningvischemia. Furthermore, our anin vitromodel using a proliferating indicate and/or intensity activating probably determines it would play beneficialvdeleterious survival