Xu Xiaodan, Zhang Hong, Wang Ke, Tu Tao, Jiang Yuan
Department of Rehabilitation Medicine, The First Affiliated Hospital of Chengdu Medical College, Chengdu 610500, China.
Department of Anesthesiology, The First Affiliated Hospital of Chengdu Medical College, Chengdu 610500, China.
Biochem Res Int. 2017;2017:5839762. doi: 10.1155/2017/5839762. Epub 2017 Feb 2.
. To observe the protective effect of edaravone (Eda) on astrocytes after prolonged exposure to carbon monoxide (CO) and further to investigate the potential mechanisms of Eda against CO-induced apoptosis. . The rat primary cultured astrocytes were cultured in vitro and exposed to 1% CO for 24 h after being cultured with different concentrations of Eda. MTT assay was used to detect the cytotoxicity of CO. Flow cytometry was used to detect the apoptosis rate, membrane potential of mitochondria, and ROS level. The mRNA and protein expressions of Bcl-2, Bax, and caspase-3 were assessed by real-time PCR and Western blotting analysis, respectively. . Eda can significantly suppress cytotoxicity of CO, and it can significantly increase membrane potential of mitochondria and Bcl-2 expressions and significantly suppress the apoptosis rate, ROS level, Bax, and caspase-3 expressions. Eda protects against CO-induced apoptosis in rat primary cultured astrocytes through decreasing ROS production and subsequently inhibiting mitochondrial apoptosis pathway.
观察依达拉奉(Eda)对长时间暴露于一氧化碳(CO)后的星形胶质细胞的保护作用,并进一步探讨Eda抗CO诱导凋亡的潜在机制。体外培养大鼠原代星形胶质细胞,用不同浓度的Eda培养后,暴露于1% CO中24小时。采用MTT法检测CO的细胞毒性。流式细胞术检测凋亡率、线粒体膜电位和ROS水平。分别通过实时PCR和Western印迹分析评估Bcl-2、Bax和caspase-3的mRNA和蛋白表达。Eda可显著抑制CO的细胞毒性,显著增加线粒体膜电位和Bcl-2表达,显著抑制凋亡率、ROS水平、Bax和caspase-3表达。Eda通过减少ROS生成并随后抑制线粒体凋亡途径来保护大鼠原代培养星形胶质细胞免受CO诱导的凋亡。