南岭柞木苷G对Aβ25-35诱导的PC12细胞损伤的保护作用

摘要

We studied the protective effect of xylocoside G on Aβ25-35-induced apoptosis in PC12 cells. Cell viability was ana-lyzed by MTT assay, and apoptotic neuronal death was assessed by Hoechst 33342 staining. Flow cytometry was used to deter-mine the apoptotic neuronal cells quantitatively. The level of intracellular reactive oxygen species (ROS) was monitored with the fluorescent probe 2',7'-dichlorofluoresce in diacetate (DCFH-DA). We found that PC12 cells treated with 25 μM Aβ25-35 for 24 h had a significant decrease in cell viability compared with control, and the percentage of apoptotic cells was increased to 34.26%. The level of intracellular oxygen species was also increased. Co-incubation with xylocoside G (10 μM) for 24 h attenuated the damaging effect of Aβ25-35 on the cell viability, and the percentage of apoptotic cells was decreased to 22.62%. Moreover, the increase of ROS induced by Aβ25-35 was inhibited by xylocoside G (10 μM). We concluded that xylocoside G had protective effect against Aβ25-35-induced apoptosis, which might be related with the decrease of the level of ROS.%研究南岭柞木苷G对β淀粉样蛋白25-35片断(Aβ<,25-35>)诱导的PC12细胞损伤的保护作用.用25 μM聚集状的Aβ<,25-35>建立神经细胞损伤模型,将培养的PC12细胞分为空白对照组,Aβ<,25-35>模型组,Aβ<,25-35>+药物组,采用MTT比色法,Hoechst33342染色法分析细胞存活率,流式细胞仪定量分析细胞凋亡率,以2',7'-二氢二氯荧光黄双乙酸钠(DCFH-DA)为标记探针检测细胞内产生的活性氧含量.(1)25μM聚集状的Aβ<,25-35>处理PC12细胞24 h能显著降低细胞活力,诱导细胞发生凋亡,凋亡率达34.26%;细胞内活性氧水平上升.(2)南岭柞木苷G与聚集状的Aβ<,25-35>共同孵育,可提高细胞存活率;流式细胞仪检测凋亡率降低到22.62%:以DCFH-DA为标记探针检测,南岭柞木苷G可明显抑制聚集状的Aβ<,25-35>引起的细胞内活性氧的产生.南岭柞木苷G能抑制Aβ<,25-35>诱导的PC12神经细胞的凋亡,其神经细胞保护作用可能与降低细胞内活性氧水平有关.