论文部分内容阅读
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 investigate the mechanism of neuronal apoptosis in acute and chronic intermittent hypoxia. Methods (1) Establishment of hypoxic animal model: SD rats were placed in atmospheric hypoxic chamber, filled with nitrogen to adjust the oxygen concentration to the required oxygen concentration. (2) Animal grouping: ① Acute hypoxia group: hypoxia 1.5h in hypoxia chamber. ② chronic intermittent hypoxia group: hypoxia every day in the 6h, 6d hypoxia each week, a total of hypoxia 28d. Apoptotic cells were detected by TdT nick end labeling (TUNEL). Results Apoptotic cells were significantly increased after acute and chronic intermittent hypoxia. Conclusion Hypoxia can induce delayed neuronal apoptosis. Hypoxic brain injury may play an important role in the pathogenesis of neurodegenerative diseases.