臂丛阻滞麻醉剂右美托咪定减轻七氟醚引起的神经细胞氧化应激和线粒体损伤  

Brachial Plexus Block Anesthetic Dexmedetomidine Reduces Sevoflurane-Induced Nerve Cell Oxidative Stress and Mitochondrial Damage

作　　者：何巍[1] 逯家宇 黄建东 He Wei;Lu Jiayu;Huang Jiandong(Department of Anesthesiology,Affiliated Hospital of Beihua University,Jilin 13201l,China)

机构地区：[1]北华大学附属医院麻醉科,吉林吉林132011

出　　处：《南开大学学报(自然科学版)》2025年第1期67-72,共6页Journal of Nankai University(Natural Sience)

基　　金：吉林省卫生与健康技术创新项目(2020J019)。

摘　　要：为了研究右美托咪定对七氟醚诱导的神经细胞损伤的保护作用及其作用机制,购买了人神经母细胞瘤SH-SY5Y细胞、小鼠海马神经元细胞HT22和原代大鼠皮层神经元细胞.采用一定浓度(2%、4%、8%)七氟醚处理细胞6 h或12 h,筛选最适七氟醚处理强度.随后,细胞分3组:对照组、七氟醚组、七氟醚+右美托咪定.CCK8检测细胞存活率,流式细胞仪检测细胞凋亡,DCFH-DA试剂盒检测ROS水平,JC-1试剂盒检测线粒体膜电位,western blot检测线粒体蛋白及JNK信号通路激活情况.细胞活力检测结果显示,神经细胞暴露于高浓度七氟醚(8%,6 h)和/或长时间七氟醚(4%/8%,12 h)后,其存活率会显著下降(P<0.05).七氟醚的临床作用强度(4%,6 h)对原代海马神经元活力没有显著影响.与对照组相比,七氟醚组神经细胞凋亡率和ROS水平显著增加,线粒体膜电位、线粒体内外膜蛋白及p-JNK蛋白表达显著下降.与七氟醚组相比,右美托咪定处理组神经细胞凋亡率和ROS水平显著减少,线粒体膜电位、线粒体内外膜蛋白及p-JNK蛋白表达显著上调.右美托咪定可有效减少七氟醚诱导的神经细胞凋亡,这可能与右美托咪定抑制ROS/JNK信号通路,从而减轻细胞氧化应激和线粒体损伤有关.To explore the protective effect and mechanism of dexmedetomidine in sevoflurane-induced nerve cell damage,the human neuroblastoma SH-SY5Y cells,mouse hippocampal neuronal cells HT22 and primary rat neurons were purchased.The cells were treated with certain concentrations(2%,4%,8%)of sevoflurane for 6 or 12 h,and screened for the optimal sevoflurane treatment intensity.Subsequently,the cells were divided into three groups:control,sevoflurane treatment,sevoflurane and dexmedetomidine treatment.CCK8 and Flow cytometry were used to detect cell survival rate and apoptosis.DCFH-DA was used to detect ROS level.The JC-1 assay kit was used to detect mitochondrial membrane potential.In addition,the mitochondrial protein and JNK signaling pathway protein expression was detected by Western blot.The results showed that long term exposure to high concentrations(8%,6 h;4%/8%,12 h)of sevoflurane resulted in a significant decrease in the survival rate of all nerve cells(P<0.05),while clinical use of sevoflurane intensity(4% sevoflurane for 6 h)did not cause a significant decrease in the vitality of primary rat hippocampal neurons.Compared with the control group,the cell apoptosis rate the cell apoptosis rate and ROS level in the sevoflurane group significantly increased,while the mitochondrial membrane potential,mitochondrial inner/outer membrane proteins,and p-JNK protein expression significantly decreased.Compared with the sevoflurane group,the dexmedetomidine treated group showed a significant decrease in cell apoptosis rate and ROS level,while the mitochondrial membrane potential,mitochondrial inner and outer membrane proteins,and p-JNK protein expression were significantly upregulated.In conclusion,dexmedetomidine alleviates sevoflurane-induced nerve cell damage by reducing cell apoptosis,which may be related to inhibition on the ROS/JNK signaling pathway,thereby alleviating cellular oxidative stress and mitochondrial damage.

关 键 词：右美托咪 七氟醚 神经损伤 氧化应激 

分 类 号：R969[医药卫生—药理学]