Diphosphorylation of extracellular signal-regulated kinases and c-Jun N-terminal protein kinases in brain ischemic tolerance in rat
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作者:
Gu, ZL
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机构:Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China
Gu, ZL
Jiang, Q
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机构:Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China
Jiang, Q
Zhang, GY
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Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R ChinaXuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China
Zhang, GY
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Cui, ZC
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机构:Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China
Cui, ZC
Zhu, ZM
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机构:Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China
Zhu, ZM
机构:
[1] Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China
[2] Dalian Med Univ, Dept Biochem, Dalian 116027, Peoples R China
Extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal protein kinases (JNKs) activation in brain ischemic tolerance were examined by Western immunoblot. ERK but not JNK diphosphorylation (activation) were increased after preconditioning ischemia. The increased JNK1 but not ERK diphosphorylation after lethal ischemia was eliminated by pretreatment with preconditioning ischemia. The results suggest that the elimination of JNK1 activation after lethal ischemia by preconditioning ischemia may be one of the important protective mechanisms in ischemic tolerance, and ERKs activation may be involved in the induction of the protective responses. (C) 2000 Elsevier Science B.V. All rights reserved.