葛根素对散发阿尔茨海默病线粒体损伤的保护作用研究

Protective effect of puerarin on mitochondrial injure in sporadic Alzheimer's disease

目的观察葛根素对散发阿尔茨海默病(SAD)线粒体损伤的保护作用。方法在无mtDNA的神经母细胞瘤细胞(SH-SY5Y cells)中转入SAD患者血小板中的mtDNA,制备SAD胞质杂交细胞模型,观察不同浓度的葛根素对该模型细胞存活率(MTT实验)、细胞凋亡(流式细胞法)及ROS水平(荧光法)的影响。结果给予葛根素(0.1～10.0μmoL/L)24 h后,SAD胞质杂交细胞的存活率分别为(76.00±3.8)%、(81.66±3.4)%和(89.67±4.5)%,有明显的浓度依赖性;并且凋亡率分别为21.83%、14.58%和14.60%,各组间差异具有统计学意义;而且SAD胞质杂交细胞的ROS水平较对照组增加(P<0.01),葛根素则能改善SAD胞质杂交细胞的ROS水平。结论葛根素通过降低细胞内ROS水平,以保护SAD线粒体。

[Objective] To investigate the protective effects of puerarin on mitochondrial injure of sporadic AD （SAD）. [Methods] SAD cybrids were created by repopulating mtDNA deficiented human neuroblastoma （SH-SY5Y） cells with mitochondria from AD patients. The effects of perarin on SAD cybrids were assessed by the assay of cell viability （MTT）, apoptosis （Annexin-V and PI staining） and endogenously ROS （CM-H2DCFDA） production. [Results] After exposure to 0.1, 1.0 or 10.0μM puerarin for 24 h, the cell viability of SAD cybrids significantly increased in a dose-dependent manner and the survival rates were （76± 3.8）%, （81.66±3.4）% and （89.67±4.5）%, respectively. The percentage of apoptotic cells was 21.83%, 14.58%, and 14.6%, respectively. The ROS level was increased in SAD cybrids, which was attanuated by the pueratin. （P〈0.01）. [Conclusion] These results suggest that puerarin protect SAD cybrids from apoptosis via scavenger of the intracellular ROS.