This research investigated the effects of eleutheroside E (EE) on the 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP)-induced Parkinson’s disease cell model and its mechanism. Methods: To create a cell model of Parkinson’s disease, MPTP (2500 μmol/L) was administered to rat adrenal pheochromocytoma cells (PC-12) to produce an MPTP group. Selegiline (50 μmol/L) and MPTP had been administered to the positive group beforehand. The eleutheroside E group was divided into low-, medium-, and high-concentration groups, in which the cells were pretreated with eleutheroside E at concentrations of 100 μmol/L, 300 μmol/L, and 500 μmol/L. Next, MPTP was added to the cells separately. The CCK-8 method was used to measure the cell survival rate. Apart from the CCK-8 method, mitochondrial membrane potential detection, cell reactive oxygen species (ROS) detection, and other methods were also adopted to verify the effect of low, medium, and high concentrations of eleutheroside E on the MPTP-induced cell model. Western blot analysis was used to detect changes in the expression of intracellular proteins CytC, Nrf2, and NQO1 to clarify the mechanism. The results are as follows. Compared with the MPTP group, the survival rates of cells at low, medium, and high concentrations of eleutheroside E all increased. The mitochondrial membrane potential at medium and high concentrations of eleutheroside E increased. The ROS levels at medium and high concentrations of eleutheroside E decreased. Moreover, the apoptosis rate decreased and the expression levels of the intracellular proteins CytC, Nrf2, and NQO1 were upregulated. Conclusion: Eleutheroside E can improve the MPTP-induced apoptosis of PC-12 cells by increasing the mitochondrial membrane potential and reducing the level of intracellular reactive oxygen species (ROS). Moreover, the apoptosis of cells is regulated by the expression of CytC, Nrf2, and NQO1 proteins.

中文翻译：

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刺五加苷E对MPTP诱导的帕金森病细胞模型的影响及其机制

本研究探讨刺五加苷E（EE）对1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的帕金森病细胞模型的影响及其机制。方法：建立帕金森病细胞模型，将MPTP（2500 μmol/L）给予大鼠肾上腺嗜铬细胞瘤细胞（PC-12），产生MPTP组。阳性组预先给予司来吉兰(50 μmol/L)和MPTP。刺五加苷E组分为低、中、高浓度组，分别用100μmol/L、300μmol/L、500μmol/L浓度的刺五加苷E预处理细胞。接下来，将 MPTP 分别添加到细胞中。采用CCK-8法测定细胞存活率。除CCK-8方法外，还采用线粒体膜电位检测、细胞活性氧（ROS）检测等方法验证低、中、高浓度刺五加苷E对MPTP诱导的细胞模型的影响。采用Western blot分析检测细胞内蛋白CytC、Nrf2和NQO1表达的变化，以阐明其机制。结果如下。与MPTP组相比，低、中、高浓度刺五加苷E下细胞的存活率均升高。中浓度和高浓度刺五加苷E时线粒体膜电位增加。中浓度和高浓度刺五加苷E的ROS水平降低。此外，细胞凋亡率下降，细胞内蛋白CytC、Nrf2和NQO1的表达水平上调。结论:刺五加苷E可通过增加线粒体膜电位、降低细胞内活性氧(ROS)水平来改善MPTP诱导的PC-12细胞凋亡。此外，细胞凋亡受CytC、Nrf2和NQO1蛋白表达的调节。