Abstract：OBJECTIVE: In order to study the mechanisms of cerebral energy failure after hypoxic-ischemic brain damage (HIBD), the effects of hypoxia-ischemia (HI) on glucose transporter proteins (GLUT1 and GLUT3) expression in the brain were investigated in neonatal rats. METHODS: Thirty seven-day-old Wistar rats were randomly assigned into Normal (n=5), Sham-operated (n=5) and HIBD model groups (n=20). The HIBD model was established by ligating the right common carotid artery combined with the hypoxia exposure (8% oxygen). The rats were sacrificed at 1,3,5 and 10 days after HIBD. The expressions of GLUT1 and GLUT3 in the brain were examined by immunohistochemistry. RESULTS: Microvascular GLUT1 was seen in the Normal group. GLUT1 immunoreactivity began to increase in ipsilateral hemisphere 1 day after HI,peaked on the 3rd day, and remained high on the 5th day. No significant changes in GLUT3 immunoreactivity were observed 1 day after HI. Three days after HI, there was a pronounced decrease in GLUT3 staining; and on the 5th day the decrease of GLUT3 staining was most significantly. The maximal decrease of GLUT3 staining was seen in the hippocampal CA1 region. CONCLUSIONS: HI may result in an abnormal expression of glucose transporter proteins in the brain, which might aggravate the neuronal injury and interfere with its repair.
XIN Ying,Vince RUSSO,George WERTHER. Expression of glucose transporter proteins in the brain of neonatal rats with hypoxic-ischemic brain damage[J]. CJCP, 2005, 7(6): 509-512.
