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Titolo:
Extracellular signal-regulated kinase and c-Jun N-terminal protein kinase in ischemic tolerance
Autore:
Gu, ZL; Jiang, Q; Zhang, GY;
Indirizzi:
Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China Xuzhou Med Coll Xuzhou Peoples R China 221002 ou 221002, Peoples R China
Titolo Testata:
NEUROREPORT
fascicolo: 16, volume: 12, anno: 2001,
pagine: 3487 - 3491
SICI:
0959-4965(20011116)12:16<3487:ESKACN>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
HIPPOCAMPAL CA1 NEURONS; RAT; ACTIVATION; BRAIN; CASCADE; GERBILS; MODEL;
Keywords:
brain; c-Jun N-terminal protein kinase; extracellular signal-regulated kinase; hippocampus; ischemic-tolerance; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
17
Recensione:
Indirizzi per estratti:
Indirizzo: Zhang, GY Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China Xuzhou Med Coll Xuzhou Peoples R China 221002 Peoples R China
Citazione:
Z.L. Gu et al., "Extracellular signal-regulated kinase and c-Jun N-terminal protein kinase in ischemic tolerance", NEUROREPORT, 12(16), 2001, pp. 3487-3491

Abstract

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) 3days 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 protectionagainst 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.

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Documento generato il 18/01/20 alle ore 01:52:51