Zhou Feng, Ju Jing, Fang Yongjun, Fan Xiaoxuan, Yan Shuguang, Wang Qiang, Wei Pengfang, Duan Fuliang, Miao Feng, Hu Zhenyuan, Wang Maode
Department of Neurosurgery, the Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, China.
Department of Neurosurgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Biotechnol Appl Biochem. 2019 Mar;66(2):247-253. doi: 10.1002/bab.1719. Epub 2018 Dec 24.
The present study aimed to investigate the protective effects of salidroside (SAL) on 1-methyl-4-phenylpyridinium (MPP )-induced PC12 cell model for Parkinson's disease. PC12 cells were pretreated with SAL in different concentrations and then exposed to MPP . To evaluate the effects of SAL on cytotoxicity, the survival rate was tested by the 3-(4,5-dimethylthiazol-2-yl)-2,5-dimethyltetrazolium bromide (MTT) assay and the apoptosis was tested via flow cytometry and Western blot. Reactive oxygen species (ROS), glutathione (GSH), and malondialdehyde (MDA) were detected to analyze the effects of SAL on oxidative stress. The mRNA and protein levels of inflammatory factors TNF-α and IL-1β were also determined by real-time quantitative polymerase chain reaction and Western blot. Pretreatment with SAL effectively relieved the MPP cytotoxic effects and decreased the release of ROS production and inflammatory cytokines. SAL also inhibited apoptosis, suppressed MDA activity, and increased GSH levels in MPP -treated PC12 cells. Moreover, the expression levels of caspase-9, caspase-3, and Bax were significantly decreased in the SAL treatment groups compared with the MPP group, whereas Bcl-2 expression was significantly increased in the SAL treatment groups. In summary, the overall results suggested that SAL have neuroprotective effects on the MPP -induced PC12 cell model by inhibiting inflammation, oxidative stress, and cell apoptosis. SAL may be a potential active product to protect against Parkinson's disease.
本研究旨在探讨红景天苷(SAL)对1-甲基-4-苯基吡啶离子(MPP⁺)诱导的帕金森病PC12细胞模型的保护作用。PC12细胞用不同浓度的SAL预处理,然后暴露于MPP⁺。为评估SAL对细胞毒性的影响,通过3-(4,5-二甲基噻唑-2-基)-2,5-二甲基四氮唑溴盐(MTT)法检测细胞存活率,并通过流式细胞术和蛋白质免疫印迹法检测细胞凋亡情况。检测活性氧(ROS)、谷胱甘肽(GSH)和丙二醛(MDA),以分析SAL对氧化应激的影响。还通过实时定量聚合酶链反应和蛋白质免疫印迹法测定炎症因子TNF-α和IL-1β的mRNA和蛋白质水平。SAL预处理有效减轻了MPP⁺的细胞毒性作用,减少了ROS生成和炎症细胞因子的释放。SAL还抑制了MPP⁺处理的PC12细胞的凋亡,抑制了MDA活性,并提高了GSH水平。此外,与MPP⁺组相比,SAL处理组中caspase-9、caspase-3和Bax的表达水平显著降低,而Bcl-2表达在SAL处理组中显著增加。综上所述,总体结果表明,SAL通过抑制炎症、氧化应激和细胞凋亡,对MPP⁺诱导的PC12细胞模型具有神经保护作用。SAL可能是一种预防帕金森病的潜在活性产物。