Increased expression of glucose transporter 3 in gerbil brains following magnesium sulfate treatment and focal cerebral ischemic injury |
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| Authors: | Chih‐Yang Huang Yi‐Fan Liou Shu‐Ying Chung Pei‐Ying Pai Chung‐Ben Kan Chia‐Hua Kuo Chang‐Hai Tsai Fuu‐Jen Tsai Jia‐Long Chen Jing‐Ying Lin |
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| Institution: | 1. Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan;2. Graduate Institute of Chinese Medicine, China Medical University, Taichung, Taiwan;3. Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan;4. Institute of Life Sciences, Central Taiwan University of Science and Technology, Taichung, Taiwan;5. Department of Nursing, Central Taiwan University of Science and Technology, Taichung, Taiwan;6. Division of Cardiology, China Medical University Hospital, Taichung, Taiwan;7. Division of Cardiovascular Surgery, Chia‐Yi Christian Hospital, Chia‐Yi, Taiwan;8. Laboratory of Exercise Biochemistry, Taipei Physical Education College, Taipei, Taiwan;9. Department of Healthcare Administration, Asia University, Taichung, Taiwan;10. Graduate Institute of Biotechnology, China Medical University, Taichung, Taiwan;11. Department of Medical Imaging and Radiological Science, Central Taiwan University of Science and Technology, Taichung, Taiwan |
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| 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 (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. |
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| Keywords: | magnesium sulfate glucose transporter 3 MEK focal cerebral ischemia |
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