七氟烷通过影响神经元能量代谢和氧化应激水平促进神经元凋亡

目的研究吸入性麻醉药七氟烷对发育期神经元的凋亡作用,并探究七氟烷对原代神经元线粒体功能的影响。方法体外培养原代神经元,并随机分为对照组和实验组,实验组用4.1%七氟烷处理6 h,western blot检测Cleaved caspase-3凋亡蛋白的变化,流式细胞术检测神经元的凋亡率,DCFH-DA法检测细胞中ROS含量的变化,并检测ATP水平的变化。结果与对照组相比,七氟烷组的凋亡蛋白Cleaved caspase-3上调(P<0.01),凋亡率增加(P<0.05),ROS生成增加(P<0.05)同时ATP生成减少(P<0.05)。结论七氟烷可以诱导原代神经元的凋亡,其作用机制可能是通过线粒体能量代谢和氧化应激水平改变引起。

Sevoflurane induces neuronal apoptosis by affecting the energy metabolism and oxidative stress

Objective This paper investigates the neurotoxic effect of the anesthetic sevoflurane,and explores the influence of the energy metabolism and oxidative stress induced by sevoflurane.Methods Primary neurons were cultured in vitro and assigned into a control group and an experimental group. The experimental group was treated with 4.1% sevoflurane for 6 hours. Western blot was used to detect the change of Cleaved caspase-3 apoptotic protein,flow cytometry was used to detect the apoptotic rates of neurons,the DCFH-DA method was used to detect the change of ROS,and ATP is also detected by test kits.Results Compared with the control group,the cleaved caspase-3 apoptotic protein in experimental group increased(P<0.01),the ROS also increased(P<0.05)but the ATP decreased(P<0.05).Conclusion The sevoflurane-induced apoptosis may be caused by mitochondrial energy metabolism.