Effect of Vitamin E on Cerebral Hypoxia-Ischemia in Neonatal Rats

ABSTRACT

PURPOSE: In order to evaluate the hypoxia-ischemia induced neurotoxic effect and the protective effect of vitamin E as an antioxidant, cell number and cell viability were measured in cerebral neurons and astrocytes derived in neonatal rats. METHODS: 7-day old neonatal rats were subjected to unilateral common carotid artery occlusion, and exposed to hypoxic condition for 3 hours. The protective effect of vitamin E, as an antioxidant was examined by XTT [2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-(phenylami-nocarbonyl) 12H-tetrazolium hydroxide] assay and cell number on 14 days after hypoxia-ischemia when the rats received an intraperitoneal injection of vitamin E immediately following hypoxia-ischemia. RESULTS: Hypoxic-ischemic condition positively decreased the cell number and cell viability of rat cerebral neurons in a time-dependent manner when rats were killed 72 hours after hypoxia- ischemia. 72 hours after hypoxia-ischemia, the cell number and viability of astrocytes were slightly decreased, compared with the saline treated group. In rats treated with vitamin E, the cell number and cell viability of neurons were significantly increased compared with those of the saline- or non-treated group. In hypoxic-ischemic treated rats after 14 days from hypoxia- ischemia, astrocytes were significantly proliferated, but vitamin E showed the protective effect on hypoxic-ischemia induced cell proliferation and cell viability. CONCLUSION: It is suggested that hypoxic-ischemic condition is more toxic in neurons than astrocytes, and selective antioxidants such as vitamin E, especially when it was administered within two hours after hypoxia-ischemia, is highly effective in preventing the cell death of neurons and astrocytes from hypoxia-ischemic condition in neonatal rats.