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目的研究慢性缺氧/再氧合对小鼠脑皮质Nip3的表达及神经细胞凋亡的影响,探索睡眠呼吸暂停综合征(SAS)脑损害的可能机制。方法自制慢性缺氧/再氧合小鼠模型:通过控制程序调控箱内氧浓度,使得每一间断性缺氧循环时间为2 min,氧浓度循环于(21.72±0.55)%与(6.84±0.47)%之间,每天缺氧/再氧合8 h。30只ICR小鼠随机分为4组:模拟对照组10只,缺氧/再氧合二周组及四周组各5只,缺氧/再氧合八周组10只。免疫组织化学方法检测小鼠额叶脑皮质Nip3的表达,TUNEL法检测脑神经细胞凋亡。结果与模拟对照组比较,缺氧/再氧合各组脑皮质Nip3的表达和凋亡神经细胞数均显著增加(P<0.05),八周组与四周组Nip3的表达和凋亡神经细胞数较二周组亦显著增加(P<0.05),八周组与四周组比较差异无统计学意义(P>0.05);脑皮质Nip3的表达与脑神经细胞凋亡之间存在正相关关系(r=0.901,P<0.05)。结论慢性缺氧/再氧合可增加脑Nip3的表达,引起皮质脑神经细胞凋亡,可能是其神经系统损害的机制之一。
Objective To investigate the effects of chronic hypoxia / reoxygenation on the expression of Nip3 and neuronal apoptosis in mouse cerebral cortex and to explore the possible mechanism of brain damage induced by sleep apnea syndrome (SAS). Methods Chronic hypoxia / reoxygenation mouse model was established. The oxygen concentration in the tank was controlled by a control program so that the intermittent hypoxia cycle time was 2 min. The oxygen concentration was cycled between (21.72 ± 0.55)% and (6.84 ± 0.47 )%, Daily hypoxia / reoxygenation 8 h. Thirty ICR mice were randomly divided into 4 groups: 10 in the simulated control group, 5 in the hypoxia / reoxygenation group and 4 weeks group, and 10 in the hypoxia / reoxygenation 8 weeks group. Immunohistochemistry was used to detect the expression of Nip3 in the frontal cortex of mice. TUNEL method was used to detect the apoptosis of brain neurons. Results Compared with the control group, the expression of Nip3 and the number of apoptotic neurons in cerebral cortex were significantly increased in hypoxia / reoxygenation group (P <0.05). The expression of Nip3 and the number of apoptotic nerve cells (P <0.05). There was no significant difference between the eight weeks group and the peripheral group (P> 0.05). There was a positive correlation between the expression of Nip3 in the cerebral cortex and the neuronal apoptosis (r = 0.901, P <0.05). Conclusion Chronic hypoxia / reoxygenation can increase the expression of brain Nip3 and cause apoptosis of cortical brain neurons, which may be one of the mechanisms of its nervous system damage.