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    宋成洁. 依达拉奉对MPP+诱导的PC12细胞氧化应激的保护作用[J]. 徐州医科大学学报, 2019, 39(12): 865-867.
    引用本文: 宋成洁. 依达拉奉对MPP+诱导的PC12细胞氧化应激的保护作用[J]. 徐州医科大学学报, 2019, 39(12): 865-867.
    Protective effect of Edaravone on mitochondrial dynamic by MPP+ in PC12 cells[J]. Journal of Xuzhou Medical University, 2019, 39(12): 865-867.
    Citation: Protective effect of Edaravone on mitochondrial dynamic by MPP+ in PC12 cells[J]. Journal of Xuzhou Medical University, 2019, 39(12): 865-867.

    依达拉奉对MPP+诱导的PC12细胞氧化应激的保护作用

    Protective effect of Edaravone on mitochondrial dynamic by MPP+ in PC12 cells

    • 摘要: 目的 探讨依达拉奉(edaravone, Eda)对MPP+诱导帕金森病(PD)细胞模型细胞线粒体氧化应激的机制研究。方法 以500 μM MPP+诱导PC12细胞损伤建立帕金森病模型,应用Eda观察ROS,脂质过氧化物质MDA,mtDNA拷贝数和ATP产生速率。结果 MPP+诱导的PD模型可增加PC12细胞ROS,脂质过氧化MDA,抑制mtDNA拷贝数和线粒体呼吸,相反,Eda可改善MPP+诱导的相关神经毒性。结论 Eda对MPP+致PC12细胞线粒体氧化应激具有保护作用,其机制可能是通过抑制脂质过氧化,恢复线粒体呼吸来实现的。

       

      Abstract: ob<x>jective Investigate the protective effect of edaravone on the Parkinson’s disease (PD) cell model and its possible mechanism, explore the effect of edaravone on MPP+-induced PC12 cells mitochondria damage protection mechanism, provide a theoretical basis on the treatment of PD. Method A model of Parkinson’s disease was established with 500 μM MPP + induced PC12 cell damage. Eda was used to observe ROS, MDA, mtDNA copy number and ATP production rate. Results MPP + -induced PD model can increase ROS, lipid peroxidation MDA, inhibit mtDNA copy number and mitochondrial respiration in PC12 cells. Conclusion Eda can improve MPP + -induced neurotoxicity. Conclusion Eda has a protective effect on mitochondrial oxidative stress induced by MPP + in PC12 cells. The mechanism may be achieved by inhibiting lipid peroxidation and restoring mitochondrial respiration.

       

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