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

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

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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	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
Description	Country affiliation: Taiwan Author Affiliation: Huang CY ( Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.)
Abstract	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. Copyright © 2010 John Wiley & Sons, Ltd.
File Format	HTM / HTML
ISSN	02636484
Issue Number	4
Volume Number	28
e-ISSN	10990844
Journal	Cell Biochemistry and Function
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2010-06-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Cell Biology Discipline Biochemistry Brain Ischemia Metabolism Glucose Transporter Type 3 Animals Chemically Induced Drug Therapy Butadienes Therapeutic Use Cerebral Cortex Enzyme Inhibitors Gerbillinae Hippocampus Magnesium Sulfate Toxicity Male Nitriles Rats Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Biochemistry Clinical Biochemistry

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Intravenous administration of MEK inhibitor U0126 affords brain protection against forebrain ischemia and focal cerebral ischemia.

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

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