Extracellular signal-regulated kinase and c-Jun N-terminal protein kinase in ischemic tolerance

被引:71
作者
Gu, ZL [1 ]
Jiang, Q [1 ]
Zhang, GY [1 ]
机构
[1] Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China
关键词
brain; c-Jun N-terminal protein kinase; extracellular signal-regulated kinase; hippocampus; ischemic-tolerance; rat;
D O I
10.1097/00001756-200111160-00023
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The alterations and involvement of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal protein kinase (JNK) activation were examined in the hippocampal CAI region in a rat model of global brain ischemic tolerance. Western blotting study showed that ERK activation (diphosphorylation) level was decreased (3.75-, 0.56-, and 0.23-fold vs sham control) and JNK activation level was increased (3.82-, 4.63-, and 5.30-fold vs sham control) 3 days after more severe ischemic insults (6min, 8min, and 10min of ischemia, respectively). These alterations were significantly prevented by pretreatment with preconditioning ischemia, which also provided neuronal protection against ischemic injury. Inhibition of ERK activation after preconditioning ischemia by PD98059, a specific ERK kinase inhibitor, significantly prevented the inhibitory effects of preconditioning ischemia on both JNK activation and ischemic injury. The results suggest that ERK activation after preconditioning ischemia may result in the prevention of JNK activation and thus be involved in the protective responses in ischemic tolerance in hippocampal CAI region. (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:3487 / 3491
页数:5
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