【摘要】 目的 探讨毛蕊花糖苷（ACT）对帕金森病（PD）细胞模型的保护作用，并揭示其可能的机制。方法 应用鱼藤酮（ROT）和6-羟基多巴胺（6-OHDA）干预PC-12和SH-SY5Y细胞构建PD细胞模型，采用MTT比色法检测不同浓度ACT对PC-12细胞活性的影响；流式细胞技术分别检测ACT对6-OHDA和ROT损伤的SH-SY5Y细胞凋亡的作用。利用激光共聚焦显微镜观察ACT对NRK和PC-12细胞线粒体自噬的影响。应用分子对接技术预测ACT与PINK1、Parkin的对接姿势和能量。结果 ACT对PC-12细胞作用24 h的IC₅₀值为695.5μM;ACT能降低ROT和6-OHDA损伤的SH-SY5Y细胞的凋亡发生率，差异有统计学意义（P<0.01）,且明显提高NRK和PC-12细胞的线粒体自噬水平；ACT对PINK1和Parkin均具有较强的对接亲和力，其亲和能量均为-9.0 kcal/mol。结论 ACT可能通过抑制细胞凋亡和调节PINK1/Parkin介导的线粒体自噬而保护PD神经细胞。更多还原

【Abstract】 Objective To explore the protective effects and the possible underlying mechanism of acteoside（ACT） on the cell model of Parkinson′s disease（PD）.Methods The PD cell model was constructed by intervening PC-12 and SH-SY5Y cells with rotenone（ROT） and 6-hydroxydopamine（6-OHDA）.MTT colorimetric assay was used to detect the effect of different concentrations of ACT on PC-12 cell activity.Flow cytometry was used to detect the effect of ACT on apoptosis of SH-SY5Y cells injured by 6-OHDA and ROT.Molecular docking techniques were used to predict the docking posture and energy of ACT with PINK1 and Parkin.Results The IC₅₀ value of ACT on PC-12 cells for 24 h was 695.5 μM.ACT decreased apoptosis rate of SH-SY5Y cells injured by 6-OHDA and ROT（P<0.01）.ACT significantly enhanced mitophagy levels of the NRK and PC-12 cells.ACT had stronger docking effects and affinity energy between both PINK1 and Parkin, both of them had the same binding energy of-9.0 kcal/mol.Conclusion ACT may protect PD neurons by inhibiting apoptosis and regulating PINK1/Parkin-mediated mitophagy.更多还原