Cheng Baohua, Guo Yunliang, Li Chuangang, Ji Bingyuan, Pan Yanyou, Chen Jing, Bai Bo
Neurobiology Institute, Jining Medical University, Jining 272067, PR China.
Shandong University School of Medicine, Jinan 250012, PR China.
J Neurol Sci. 2014 Aug 15;343(1-2):115-9. doi: 10.1016/j.jns.2014.05.051. Epub 2014 Jun 2.
Oxidative stress is involved in the pathogenesis of Parkinson's disease (PD). Edaravone has been shown to have a neuroprotective effect. In the present work, we investigated the effect of edaravone on 1-methyl-4-phenylpyridinium (MPP(+))-treated PC12 cells. Edaravone inhibited the decrease of cell viability and apoptosis induced by MPP(+) in PC12 cells. In addition, edaravone alleviated intracellular reactive oxygen species (ROS) production. MPP(+) induced heme oxygenase-1 (HO-1) expression, which was further enhanced by edaravone. The inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of edaravone. So edaravone protected PC12 cells against MPP(+)-cytoxicity via inhibiting oxidative stress and up-regulating HO-1 expression. The data showed that edaravone was neuroprotective and could be potentially therapeutics for PD in future.
氧化应激参与帕金森病（PD）的发病机制。依达拉奉已被证明具有神经保护作用。在本研究中，我们研究了依达拉奉对1-甲基-4-苯基吡啶离子（MPP(+)）处理的PC12细胞的影响。依达拉奉抑制了MPP(+)诱导的PC12细胞活力下降和凋亡。此外，依达拉奉减轻了细胞内活性氧（ROS）的产生。MPP(+)诱导血红素加氧酶-1（HO-1）表达，依达拉奉进一步增强了这种表达。HO-1抑制剂锌原卟啉-IX减弱了依达拉奉的神经保护作用。因此，依达拉奉通过抑制氧化应激和上调HO-1表达来保护PC12细胞免受MPP(+)的细胞毒性。数据表明依达拉奉具有神经保护作用，未来可能成为治疗PD的药物。
