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標題: Molecules involve in the self-protection of neurons against glucose-oxygen-serum deprivation (GOSD)-induced cell damage
作者: Wang, C.H.
Lee, W.J.
Ghanta, V.K.
Wang, W.T.
Cheng, S.Y.
Hsueh, C.M.
關鍵字: GOSD;Neurotrophic factors;Inflammatory factors;Leptin;Superoxide;NO;activated protein-kinase;in-vitro ischemia;nitric-oxide;cyclooxygenase-2 expression;oxidative stress;inflammatory response;cerebral-ischemia;cortical-neurons;up-regulation;brain-cells
Project: Brain Research Bulletin
期刊/報告no:: Brain Research Bulletin, Volume 79, Issue 3-4, Page(s) 169-176.
Molecules involved in self-protection of neurons against glucose/oxygen/serum deprivation (GOSD) were investigated. Trypan blue dye exclusion assay, Western blotting, ELISA, cytokine antibody array and chemical blocking assay were applied in the study. Results showed that early induction (at 6 h of GOSD) of cyclooxygenase-2 (COX-2), leptin, transforming growth factor-beta 1 (TGF-beta 1), glial-cell-line-derived neurotrophic factor (GDNF) and neurotrophin-3 (NT-3) all played a compensatory role in the protection of neurons against GOSD. Decline of these molecules and peroxisome proliferators-activated receptor (PPAR)-gamma and -alpha since 12 h of GOSD may lead to an irreversible neuronal death. Nitric oxide (NO) and superoxide at low concentrations were neuroprotective whereas at high concentrations were detrimental to neurons. Accumulation of NO and superoxide at late stage of GOSD should therefore be prevented. The study provided a useful platform for screening of potential anti-ischemic drugs and also explained why GOSD neuron derived conditioned medium (NCM) only exerted a time-restricted neuroprotection. (C) 2009 Elsevier Inc. All rights reserved.
ISSN: 0361-9230
DOI: 10.1016/j.brainresbull.2009.02.006
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