Increased expression of glucose transporter 3 in gerbil brains following magnesium sulfate treatment and focal cerebral ischemic injury

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題名:	Increased expression of glucose transporter 3 in gerbil brains following magnesium sulfate treatment and focal cerebral ischemic injury
作者:	黃志揚;HUANG, CHIH-YANG;Liou, Yi-Fan;Chung, Shu-Ying;Pai, Pei-Ying;Kan, Chung-Ben;Kuo, Chia-Hua;Tsai, Chang-Hai;Tsai, Fuu-Jen;Chen, Jia-Long;Lin, Jing-Ying
貢獻者:	生物科技學系
關鍵詞:	magnesium sulfate;glucose transporter 3;MEK;focal cerebral ischemia magnesium sulfate;glucose transporter 3;MEK;focal cerebral ischemia
日期:	2010-06
上傳時間:	2012-11-23 09:13:16 (UTC+0)
摘要:	Glucose is the primary energy substrate for neurons. Glucose transporter 3 (Glut3) localizes at the neuronal cellular membrane, which transports glucose from the extracelluar space into neurons. Ischemia results in an increased energy demand that is associated with profound changes in brain energy metabolism. Magnesium sulfate (MgSO(4)) ameliorates ischemia-induced neuronal death in the rat and gerbil model. We investigated the effects of MgSO(4) administration on the expression of Glut3 in cortex and hippocampus of gerbils during ischemia. The focal cerebral ischemia was produced by unilateral occlusion of the right common carotid artery and right middle cerebral artery. Following ischemia, Glut3 expression increased significantly versus non-ischemic (contra-lateral) cortex and hippocampus. MgSO(4) treatment significantly increased the level of Glut3 expression in the non-ischemic and ischemic cortex and hippocampus. We found that the MgSO(4)-induced increase in Glut3 expression was not reversed by administration of U0126, a MEK kinase inhibitor. These results suggest that other factors may function to modulate the MgSO(4)-induced Glut3 response. In all, our data showed that MgSO(4) increases the expression of Glut3 in the cortex and hippocampus of gerbil brains both in non-ischemia and ischemia status. However, the MEK signaling pathway might not be involved in MgSO(4)-induced Glut3 expression following focal ischemia. Glucose is the primary energy substrate for neurons. Glucose transporter 3 (Glut3) localizes at the neuronal cellular membrane, which transports glucose from the extracelluar space into neurons. Ischemia results in an increased energy demand that is associated with profound changes in brain energy metabolism. Magnesium sulfate (MgSO4) ameliorates ischemia-induced neuronal death in the rat and gerbil model. We investigated the effects of MgSO4 administration on the expression of Glut3 in cortex and hippocampus of gerbils during ischemia. The focal cerebral ischemia was produced by unilateral occlusion of the right common carotid artery and right middle cerebral artery. Following ischemia, Glut3 expression increased significantly versus non-ischemic (contra-lateral) cortex and hippocampus. MgSO4 treatment significantly increased the level of Glut3 expression in the non-ischemic and ischemic cortex and hippocampus. We found that the MgSO4-induced increase in Glut3 expression was not reversed by administration of U0126, a MEK kinase inhibitor. These results suggest that other factors may function to modulate the MgSO4-induced Glut3 response. In all, our data showed that MgSO4 increases the expression of Glut3 in the cortex and hippocampus of gerbil brains both in non-ischemia and ischemia status. However, the MEK signaling pathway might not be involved in MgSO4-induced Glut3 expression following focal ischemia. Copyright © 2010 John Wiley & Sons, Ltd.
關聯:	CELL BIOCHEMISTRY AND FUNCTION
顯示於類別:	[生物科技學系] 期刊論文

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