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흰쥐에서 허혈성 뇌경색에 대한 에스트로겐의 신경보호 효과
김원회(Won Whe Kim),이규섭(Kyu Sup Lee),최영철(Yeong Cheul Choi),신병섭(Byung Sup Shin),김기형(Ki Hyung Kim) 대한폐경학회 2002 대한폐경학회지 Vol.8 No.1
N/A Objective: Overall incidence of stroke is uniformly higher in men than in women, and rare especially in women during the reproductive stage. A number of studies have demonstrated the reduced infarct size upon administration of estrogen to ovariectomized females in ischemic brain injury models. Design: We aimed to examine the potential neuroprotective effects of 17 beta-estradiol on the cerebral infarct size and then on the apoptotic mechanism after the completion of 2-hour occlusion of middle cerebral artery (MCA) and 24-hour reperfusion. Results: The ischemic zone with cerebral infarct was consistently observed in the cortex and striatum of the left hemisphere at 24 hours of reperfusion after the completion of 2-hour occlusion of left MCA. The infarct area and volume were significantly reduced, when rats received 4 and 10 mg/kg 17 β-estradiol intraperitoneally 24 hours before and 5 min after 2-hour ischemia. Samples from the regions corresponding to the penumbra showed markedly reduced Bcl-2 protein level and, in contrast, high levels of Bax protein and cytochrome c release. Both increased Bax and cytochrome c were significantly reduced, and decreased Bcl-2 protein was markedly restored by 17 β-estradiol. 17 β-estradiol(10-1-10-5M) potently scavenged hydroxyl radicals and inhibited intracellular hydrogen peroxide production. Conclusion: 17 β-estradiol treatments decrease ischemic brain infarction in association with inhibition of apoptotic cell death.
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