【摘 要】
：
间歇性低氧(intermittent hypoxia,IH)可通过氧化应激和炎症反应诱导认知障碍,而不同频率的IH刺激可对特定类型的细胞引起不同结果.因此本研究旨在比较3种频率IH刺激对海马神
【机 构】
：
河北中医学院生理学教研室,石家庄050200
论文部分内容阅读
间歇性低氧(intermittent hypoxia,IH)可通过氧化应激和炎症反应诱导认知障碍,而不同频率的IH刺激可对特定类型的细胞引起不同结果.因此本研究旨在比较3种频率IH刺激对海马神经元HT22细胞活性的影响,探讨IH刺激损伤神经元的相关分子机制.体外培养HT22细胞,分为对照组和3个不同频率IH刺激组(舱内氧浓度在21％和1％之间循环,IHl组:6循环/h;IH2组:2循环/h;IH3组:0.6循环/h).分别在IH刺激6、12、24和48 h观察细胞形态,采用CCK-8试剂盒测定细胞活性,用试剂盒测定细胞上清中乳酸脱氢酶(lactate dehydrogenase,LDH)含量,用DCFH-DA探针检测细胞内活性氧(reactive oxygen species,ROS)水平,用Western blot检测低氧诱导因子lα(hypoxia inducible factor-l α,Hif-lα)和核因子κB(nuclear factor kappaB,NF-κB)的表达水平.结果显示,与对照组相比,3个IH处理组细胞数量均减少.随IH刺激时间延长,IH处理组细胞活性均呈现不同程度的降低,细胞培养基上清中LDH含量增加,细胞内ROS水平提高,且以IH1组变化最为明显;Hif-lα蛋白表达水平和p-NF-κB/NF-κB比值也随IH刺激时间延长而升高,以IH1组变化最为显著.以上结果提示,IH刺激可导致HT22细胞氧化应激损伤,其机制与Hif-lα表达上调以及NF-κB磷酸化水平提高有关,并且高频率的IH刺激对细胞损伤更为显著.
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