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뇌의 재관류손상에서 bcl-2와 ba 발현양상과 apoptosis의 상관관계
황성규,손윤경,성주경,변승엽,함인석,김승래 경북대학교 병원 2003 경북대학교병원의학연구소논문집 Vol.7 No.1
Background: Delayed neuronal injury strikes more damage on the survived neurons at the time on the injury. The apoptosis is known to play a major role in the pathogenesis of the second neuronal injury. Prevention of the secondary neural injury is another very important target to save the neuron in stroke. In this regards, authors conducted this experiment to elucidate the chronological changes of the apoptosis in association with the expression of bel-2-and bax. Material and Methods : Middle cerebral arteries of Spraque.Dawley rats weighing 300-400 gm were occluded for 2 hours using 4-0 nylon intro-duced-from the external carotid arteries. Light microscopic examination, TUNEL, and immuno histochemistry for cel-2 and were performed at 3 hours, 1 and 3 days, and 2 weeks after reperfusion. Results : most severe infarction were found at one day after reperfusion, thereafter progressively decreased. Apoptosis examined by TUNEL appeared from 3 hours after reperfusion, persisted for 3 days, and decreased thereafter. Expression of bcl-2 and bax paralleled the course of the apoptosis. Conclusion : Delayed neuronal injury due to apoptosis progresses for more than 3 days after the reperfusion. Appropriate measures in the early stage can contribute to prevent the neuronal injury after stroke.
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