碩士 / 中臺科技大學 / 生命科學研究所 / 96 / Background. Cerebral stroke is a cause of death and disability. Previous studies have demonstrated that magnesium has cytoprotective properties for treating experimental rat brain injuries, however the information and mechanisms regarding the protective effects of magnesium sulfate on neurons still remains unclear. The brain type glucose transporter GLUT3 (glucose transporter 3) is mainly located neuron plasma membrane and contributes to glucose transport into neuronal cells as the major usage of energy source to maintain neuron survival. Evidences also showed that ERK (extracellular signal-regulated kinase), CREB (cyclic AMP response element-binding protein) protein promote neuronal survival in the face of global ischemia. In the present study, we further evaluate the effects of magnesium sulfate on regulation of GLUT3, ERK protein and apoptosis during experimental focal cerebral ischemia. Methods. The experiments were conducted on male gerbils at 8 weeks of age, weighing 65-80g. The gerbils colonies were housed under 12-h light/dark cycles at 26 °C and fed regular chow and tap water. Gerbils at 8 weeks of age randomly were divided into 4 groups. Focal cerebral ischemia was induced by occlusion of the right common carotid artery and right middle cerebral artery (CCA + MCA) for 60 min and 30 min. Magnesium sulfate (90 mg/kg, i.p) and saline were given 30 min prior to the occlusion. Experiments were performed by TTC assays and western blotting assays. Results. Magnesium sulfate treatment significantly upregulated GLUT3 protein and anti-apoptotic Bcl-2 protein, and activated ERK protein. Magnesium sulfate treatment significantly decreased (CCA + MCA)-induced the expression of pro-apoptotic Bad, Bax, caspase-9 and caspase-3 in cortex. Conclusions. These studies demonstrated that magnesium sulfate provides significant neuroprotection in a gerbil model of focal cerebral ischemia by the increases in GLUT3 and anti-apoptotic Bcl-2, the reduction of pro-apoptotic proteins (e.g. Bad, Bax, caspas-9 and caspase-3), the activation of ERK protein. These findings may provide one of possible therapeutic approach for potential treatment or preventing stroke.
| Identifer | oai:union.ndltd.org:TW/096CTC05105005 |
| Date | January 2008 |
| Creators | Yi-Fan Liu, 劉憶帆 |
| Contributors | Jing-Ying Lin, 林靜瑩 |
| Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
| Language | zh-TW |
| Detected Language | English |
| Type | 學位論文 ; thesis |
| Format | 72 |
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