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右美托咪定对谷氨酸所致PC12细胞损伤的保护作用及其机制

张卫东 张浩 汪海 张娜 杜春彦 余军 冯泽国

南方医科大学学报2017,Vol.37Issue(2):150-156,7.
南方医科大学学报2017,Vol.37Issue(2):150-156,7.DOI:10.3969/j.issn.1673-4254.2017.02.02

右美托咪定对谷氨酸所致PC12细胞损伤的保护作用及其机制

Protective effect of dexmedetomidine against glutamate-induced cytotoxicity in PC12 cells and its mechanism

张卫东 1张浩 2汪海 2张娜 1杜春彦 1余军 1冯泽国1

作者信息

  • 1. 解放军总医院麻醉手术中心,北京100853
  • 2. 军事医学科学院卫生与环境研究所,北京100850
  • 折叠

摘要

Abstract

Objective To investigate the protective effects of dexmedetomidine (Dex) against glutamate-induced cytotoxicity in PC12 cells and its mechanism.Methods PC12 cells were treated with varying concentrations of dexmedetomidine 1 h before exposure to a high concentration of glutamate.The cell viability was measured by MTT assay,and LDH release,MDA content and SOD activity were measured.The level of ROS was tested by DCFH-DA staining and flow cytometry.The level of intracellular Ca2+ was detected by Fluo-8 staining and flow cytometry,and the mitochondrial membrane potential (MMP) was determined with JC-1 staining and flow cytometry.Results Within the concentration range of 0.01 to 100 μrnol/L,Dex dose-dependently protected PC12 cells against glutamate-induced cytotoxicity.Treatment with 100 μmol/L Dex significantly increased the cell viability to (86.6±2.2)% of that of the control cells (P<0.01) and decreased LDH release to 1.4±0.1 folds of the control level (P<0.01).In PC12 cells exposed to glutamate,Dex pretreatment significantly reduced MDA content (P<0.01),enhanced SOD activity (P<0.01),inhibited ROS overproduction (P<0.01),reduced intracellular Ca2 + level (P<0.01) and maintained a stable MMP (P<0.01).Conclusion Dexmedetomidine can protect PC12 cells against glutamate-induced injury possibly in relation with its anti-oxidative activity,inhibitory effect on intracellular calcium overload and protective effect of the mitochondria.

关键词

右美托咪定/PC12细胞/谷氨酸

Key words

dexmedetomidine/PC12 cells/glutamate

引用本文复制引用

张卫东,张浩,汪海,张娜,杜春彦,余军,冯泽国..右美托咪定对谷氨酸所致PC12细胞损伤的保护作用及其机制[J].南方医科大学学报,2017,37(2):150-156,7.

基金项目

国家973项目(2012CB518200) (2012CB518200)

军队“十二五”重大专项(AWS11J003)Supported by National Key Basic Research Program (2012CB518200). (AWS11J003)

南方医科大学学报

OA北大核心CSCDCSTPCDMEDLINE

1673-4254

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