RESUMEN
PURPOSE: To investigate the effect of intraperitoneal injection of IGF-I after hypoxic ischemic brain injury on neuronal cell necrosis, apoptosis and expression of proapoptotic and antiapoptotic proteins bax and bcl-2, respectively. METHODS: The right carotid artery was cut between the double ligation. Then allowed to recover for 30 minutes followed by exposure to 8% oxygen at 37degree C for 2 hours. Devided 2 groups, control group(N=30) and IGF-I treated group(N=30). IGF-I treated group received IGF-I 20 microg 2 hours after hypoxic ischemic injury intraperitoneally. Rates were decapitated at 24 hours and 72 hours following hypoxic ischemic brain injury. After then, right hippocampal CA1 and CA3 neuronsof rat brains were examined. RESULTS: The apoptosis and necrosis was significantly less in IGF-I treated group than control group and necrosis was more prominent in CA1 neurons than CA3 neurons. Necrosis was slightly decreased at 72 hours in both groups(P<0.05). The apoptosis was more prominent at 24 hours than 72 hours after hypoxic ischemic injury(P<0.05). Bax protein expression was prominent in control group, especially at 72 hours(P<0.05) and less in the IGF-I treated group than control group. Bcl-2 protein expression was not detected in both group. CONCLUSION: The results from this study suggest that exogenous systemic IGF-I had a neuroprotective effect by inhibition of up-regulation of bax protein expression after hypoxic ischemic brain injury.