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慢性间断性缺氧诱导大脑细胞凋亡的研究 被引量:22

Study of the apoptosis in rat brain induced by chronic intermittent hypoxia
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摘要 目的 探讨急性及慢性间断性缺氧时大脑神经细胞凋亡的机制。方法  (1)建立缺氧动物模型 :将SD大鼠置于常压低氧舱中 ,充入氮气调节氧浓度至所需氧浓度。 (2 )动物分组 :①急性缺氧组 :在低氧舱中缺氧1.5h。②慢性间断性缺氧组 :每日在低氧舱中 6h ,每周缺氧 6d ,共缺氧 2 8d。采用原位TdT缺口末端标记(TUNEL)法检测凋亡细胞。结果 急性及慢性间断性缺氧后凋亡细胞明显增加。结论 缺氧可诱导迟发性神经细胞凋亡。缺氧性脑损伤可能在神经系统变性疾病的发病机制中起重要作用。 Objective To determine whether an established models of acute and chronic cerebral hypoxia in the rats demonstrates any features of apoptosis.Methods (1)To establish the animal model of hypoxia,male Sprague Dawley rats were placed in a chamber maintained at 10% O 2.Hypoxia was maintained by infusing N 2 balanced against an inward leak of air through holes in the chamber.(2)The rats were divided into two groups:acute hypoxia group and chronic hypoxia group.The rats of acute hypoxia group were placed in the hypoxic chamber for 1.5 hour while the chronic hypoxic rats were 6 hour of hypoxia daily (6 days/week,4 weeks).After the hypoxic models were made,The severity of hypoxic damage was assessed in the cortex and hippocampus by light microscpy.Apoptosis was examined by using terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL).Results Apoptosis occurred both in acute and chronic hypoxia group.The peak of apoptosis was seen at 5th day after hypoxia,which was more than that of chronic hypoxia group.Apoptotic cells were mostly distributed in the cortex and hippocampus.Conclusions The results indicated that apotposis occurred after being exposed to hypoxia.Hypoxic cerebral injury might play an important role in the pathogenesis of neurodegenerative disease.
出处 《北京医学》 CAS 北大核心 2002年第5期339-341,共3页 Beijing Medical Journal
关键词 细胞凋亡 低氧 脑损害 发病机制 缺氧性脑损伤 动物模型 Hypoxia Cerebral injury Apoptosis
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