间歇性低氧干预对脑缺血大鼠神经功能恢复的影响

目的:探究脑缺血后间歇性低氧干预的神经保护作用及机制。方法:8周龄雄性Sprague-Dawley（SD）大鼠随机分为假手术组（SHAM，n=6）、脑缺血-静息组（MCAO-SED，n=7）和脑缺血-间歇性低氧组（MCAO-IH，n=7）。术后1周开始对MCAO-IH组进行低氧干预，持续4周。每周进行改良神经损伤程度评分（mNSS）；干预4周后采用MRI检测大鼠脑梗死体积；Western 印迹法检测脑皮质梗死边缘区脑组织腺苷酸活化蛋白激酶（AMPK）和过氧化物酶体增殖物激活受体γ辅激活因子-1α（PGC-1α）的表达量。 结果:与MCAO-SED组相比，MCAO-IH组死亡率无差异（14.29%，P>0.05）；mNSS评分显著降低（P<0.05）；脑梗死体积明显减小（P<0.01）；梗死边缘区AMPK和PGC-1α表达量显著升高（PAMPK<0.001，PPGC-1α<0.05）。相关性分析结果显示，梗死边缘区AMPK和PGC-1α表达量与mNSS评分之间均呈显著负相关（P<0.05）。结论:间歇性低氧干预可通过上调脑组织中AMPK和PGC-1α蛋白表达，进而减小脑梗死体积，促进运动功能恢复，可能通过激活AMPK/PGC-1α信号通路发挥神经保护作用。

Effect of intermittent hypoxic intervention on neurological function recovery in cerebral ischemic rats

Objective: To explore the neuroprotective effect and mechanism of intermittent hypoxia intervention after cerebral ischemia.Methods: 8-week male Sprague-Dawley（SD） rats were randomly divided into sham operation group（SHAM，n=6），MCAO-Sedentary group （MCAO-SED，n=7） and MCAO-Intermittent Hypoxia group（MCAO-IH，n=7）. In MCAO-IH group，hypoxia was conducted 1 week after operation and lasted for 4 weeks. The modified neurological severity score（mNSS） was performed weekly. After 4 weeks of intervention，MRI was used to detect cerebral infarct volume in rats; Western blotting was used to detect the expression of AMPK and PGC-1α in the peri-infarction region. Results: Compared with MCAO-SED group，MCAO-IH group performed the same mortality rate（14.29%，P>0.05），decreased mNSS score（P<0.05），decreased infarct volume（P<0.01），and increased the expression of AMPK and PGC-1α（PAMPK<0.001，PPGC-1α<0.05）. Correlation analysis results showed that the expression of AMPK and PGC-1α in the peri-infarction region were significantly negatively correlated with mNSS score（P<0.05）. Conclusion:Intermittent hypoxia can increase the expression of AMPK and PGC-1α in brain tissue，thereby reducing the infarct volume and promoting the recovery of motor function after cerebral ischemia. It may play a neuroprotective role by activating AMPK/PGC-1α signaling pathway.