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Merck
  • Molecules involve in the self-protection of neurons against glucose-oxygen-serum deprivation (GOSD)-induced cell damage.

Molecules involve in the self-protection of neurons against glucose-oxygen-serum deprivation (GOSD)-induced cell damage.

Brain research bulletin (2009-05-12)
Chen-Hsuan Wang, Wen-Jane Lee, Vithal K Ghanta, Wei-Ti Wang, Shu-Yun Cheng, Chi-Mei Hsueh
摘要

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 6h of GOSD) of cyclooxygenase-2 (COX-2), leptin, transforming growth factor-beta1 (TGF-beta1), 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 12h 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.

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Sigma-Aldrich
GW9662, >98% (HPLC)
Sigma-Aldrich
羧基-PTIO 钾盐
Sigma-Aldrich
NS-398, ≥98% (HPLC), solid
Sigma-Aldrich
2-氨基嘌呤 硝酸盐, ≥99%