Activation of Akt/FoxO and inactivation of MEK/ERK pathways contribute to induction of neuroprotection against transient global cerebral ischemia by delayed hypoxic postconditioning in adult rats

Neuropharmacology

Volumn 63, Issue 5, 2012, Pages 873-882

  Zhan, Lixuan ^a   Li, Danfang ^a   Liang, Donghai ^b   Wu, Baoxing ^a   Zhu, Pingping ^a   Wang, Yanmei ^a   Sun, Weiwen ^a   Xu, En ^a  

^a GUANGZHOU MEDICAL UNIVERSITY   (China)

^b PEKING UNIVERSITY   (China)

Author keywords

Cerebral ischemia; Hypoxia; Neuroprotection; Postconditioning; Signal pathways

Indexed keywords

1,4 DIAMINO 1,4 BIS(2 AMINOPHENYLTHIO) 2,3 DICYANOBUTADIENE; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE KINASE; PROTEIN KINASE B; TRANSCRIPTION FACTOR FOXO;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DRUG EFFECT; ENZYME ACTIVATION; ENZYME INACTIVATION; ENZYME PHOSPHORYLATION; HIPPOCAMPAL CA1 REGION; ISCHEMIC POSTCONDITIONING; ISCHEMIC PRECONDITIONING; MALE; NERVE CELL LESION; NERVE CELL NECROSIS; NEUROPROTECTION; NONHUMAN; PRIORITY JOURNAL; RAT; TRANSIENT ISCHEMIC ATTACK;

ANIMALS; CA1 REGION, HIPPOCAMPAL; CELL DEATH; CEREBROVASCULAR CIRCULATION; DOWN-REGULATION; ENZYME ACTIVATION; ENZYME INHIBITORS; FORKHEAD TRANSCRIPTION FACTORS; ISCHEMIC ATTACK, TRANSIENT; ISCHEMIC POSTCONDITIONING; MALE; MAP KINASE SIGNALING SYSTEM; NERVE TISSUE PROTEINS; NEURONS; PHOSPHATIDYLINOSITOL 3-KINASES; PHOSPHORYLATION; PROTEIN PROCESSING, POST-TRANSLATIONAL; PROTO-ONCOGENE PROTEINS C-AKT; RANDOM ALLOCATION; RATS; RATS, WISTAR; TIME FACTORS;

EID: 84864440352     PISSN: 00283908     EISSN: 18737064     Source Type: Journal    
DOI: 10.1016/j.neuropharm.2012.06.035     Document Type: Article

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