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.
