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

被引:10
作者
Wang, Chen-Hsuan [1 ,2 ]
Lee, Wen-Jane [3 ]
Ghanta, Vithal K. [4 ]
Wang, Wei-Ti [1 ]
Cheng, Shu-Yun [1 ]
Hsueh, Chi-Mei [1 ]
机构
[1] Natl Chung Hsing Univ, Dept Life Sci, Taichung 40227, Taiwan
[2] Natl Taiwan Sport Univ, Dept Adapted Phys Educ, Tao Yuan 33301, Taiwan
[3] Taichung Vet Gen Hosp, Dept Educ & Res, Taichung 407, Taiwan
[4] Univ Alabama Birmingham, Dept Biol, Birmingham, AL 35294 USA
关键词
GOSD; Neurotrophic factors; Inflammatory factors; Leptin; Superoxide; NO; ACTIVATED PROTEIN-KINASE; NITRIC-OXIDE; CYCLOOXYGENASE-2; EXPRESSION; INFLAMMATORY RESPONSE; OXIDATIVE STRESS; CORTICAL-NEURONS; UP-REGULATION; BRAIN-CELLS; LEPTIN; NEUROPROTECTION;
D O I
10.1016/j.brainresbull.2009.02.006
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
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 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.
引用
收藏
页码:169 / 176
页数:8
相关论文
共 35 条
[1]   Human immunodeficiency virus-1/surface glycoprotein 120 induces apoptosis through RNA-activated protein kinase signaling in neurons [J].
Alirezaei, Mehrdad ;
Watry, Debbie D. ;
Flynn, Claudia F. ;
Kiosses, William B. ;
Masliah, Eliezer ;
Williams, Bryan R. G. ;
Kaul, Marcus ;
Lipton, Stuart A. ;
Fox, Howard S. .
JOURNAL OF NEUROSCIENCE, 2007, 27 (41) :11047-11055
[2]   Cyclooxygenase-2 inhibitor NS-398 protects neuronal cultures from lipopolysaccharide-induced neurotoxicity [J].
Araki, E ;
Forster, C ;
Dubinsky, JM ;
Ross, ME ;
Iadecola, C .
STROKE, 2001, 32 (10) :2370-2375
[3]   PPAR:: a new pharmacological target for neuroprotection in stroke and neurodegenerative diseases [J].
Bordet, R. ;
Ouk, T. ;
Petrault, O. ;
Gele, P. ;
Gautier, S. ;
Laprais, M. ;
Deplanque, D. ;
Duriez, P. ;
Staels, B. ;
Fruchart, J. C. ;
Bastide, M. .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2006, 34 :1341-1346
[4]   Neuroprotection of cultured cortical neurons mediated by the cyclooxygenase-2 inhibitor APHS can be reversed by a prostanoid [J].
Carlson, NG .
JOURNAL OF NEUROSCIENCE RESEARCH, 2003, 71 (01) :79-88
[5]   The conditioned enhancement of neutrophil activity is catecholamine dependent [J].
Chao, HJ ;
Hsu, YC ;
Yuan, HP ;
Jiang, HS ;
Hsueh, CM .
JOURNAL OF NEUROIMMUNOLOGY, 2005, 158 (1-2) :159-169
[6]   Zinc toxicity on neonatal cortical neurons: involvement of glutathione chelation [J].
Chen, CJ ;
Liao, SL .
JOURNAL OF NEUROCHEMISTRY, 2003, 85 (02) :443-453
[7]   Cyclooxygenase-2 activity contributes to neuronal expression of cyclin D1 after anoxia/ischemia in vitro and in vivo [J].
Chen, RW ;
Zhang, YQ ;
Rose, ME ;
Graham, SH .
MOLECULAR BRAIN RESEARCH, 2004, 132 (01) :31-37
[8]   Oxidative stress and inflammatory response evoked by transient cerebral ischemia/reperfusion:: Effects of the PPAR-α agonist WY14643 (vol 41, pg 579, 2006) [J].
Collino, Massimo ;
Aragno, Manuela ;
Mastrocola, Raffaella ;
Benetti, Elisa ;
Gallicchio, Margherita ;
Dianzani, Chiara ;
Danni, Oliviero ;
Thiemermann, Christoph ;
Fantozzi, Roberto .
FREE RADICAL BIOLOGY AND MEDICINE, 2006, 41 (10) :1619-1619
[9]   Neuroprotective effects of leptin in vivo and in vitro [J].
Dicou, E ;
Attoub, S ;
Gressens, P .
NEUROREPORT, 2001, 12 (18) :3947-3951
[10]   Increased vulnerability of neuronal cell lines to sodium nitroprusside-mediated toxicity is caused by the decreased level of nitric oxide metabolites [J].
Ghosh, C ;
Lahiri, DK .
JOURNAL OF MOLECULAR NEUROSCIENCE, 1999, 13 (1-2) :77-92