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Effect Of Exogenoux Carbon Monoxide Against Heme Oxygenase System Of Astroglial Cell Cultured In Vitro

Posted on:2007-12-13Degree:MasterType:Thesis
Country:ChinaCandidate:Y L ZhuFull Text:PDF
GTID:2144360185470510Subject:Neurology
Abstract/Summary:PDF Full Text Request
Objective Pathogenesis of Carbon Monoxide Poisoning (COP) and Delayed Encephalopathy After Carbon Monoxide Poisoning(DEACMP) is very complicated, and the exact mechanism still remains unclear. Prior studies have shown that the organism itself can degenerate endogenous carbon monoxide(CO) and it is believed to be another important member of the gaseous messenger in vivo except nitrogen monoxidum(NO). There are at least two pathways in vivo to generate CO: One is oxidation of polar molecule ; Another one is the disassociation of haem by haem oxygenase(HO), The second one is the main path. So HO-CO system is increasingly concerned. In recent years some studies indicate that the induction of HO-1 is a adaptative reaction against oxidative stress, and the up-regulation of HO-1 is observed in various brain injury. Because exogenoux CO and endogenous CO are the same chemical materials, in COP the variation and the function of HO-CO system, as the ingredient of organism defense system, are needed to be discussed. At present the study about the function of the variation of CO messenger system in pathogenesis of COP is barly, and it is still in the hypothetic stage. The effect of exogenoux CO to HO-CO system of astroglial cells of wistar rat cerebral cortex cultured in vitro is not yet reported .In this paper, astroglial cells of wistar rat cerebral cortex cultured in vitro are cultivated with CO,depleting the effect of hypoxia, to observe the effect of CO to HO-CO system and its function, to explore the function of the variation of HO-CO system in the brain injury after COP at the point of view of glial cell, and to provide a clue to the exact mechanism of COP and DEACOP.
Keywords/Search Tags:carbon monoxide, heme oxygenase, astroglial cell, apoptosis
PDF Full Text Request
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