We studied the protective effect of xylocoside G on Aβ25-35-induced apoptosis in PC12 cells. Cell viability was analyzed by MTT assay, and apoptotic neuronal death was assessed by Hoechst 33342 staining. Flow cytomet...We studied the protective effect of xylocoside G on Aβ25-35-induced apoptosis in PC12 cells. Cell viability was analyzed by MTT assay, and apoptotic neuronal death was assessed by Hoechst 33342 staining. Flow cytometry was used to determine the apoptotie 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 pM 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 （10μM） for 24 h attenuated the damaging effect of Aβ25-5 on the cell viability, and the percentage of apoptotic cells was decreased to 22.62%. Moreover, the increase of ROS induced by Aβ25-5 was inhibited by xylocoside G （10μM）. 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.展开更多
基金Changjiang Scholar and Innovative Team in University (Grant No. 985-2-063-112)National Natural Science Foundation of China (Grant No. 30570533 and 30670414)China 973 Project (Grant No. 2006CB500705)
文摘We studied the protective effect of xylocoside G on Aβ25-35-induced apoptosis in PC12 cells. Cell viability was analyzed by MTT assay, and apoptotic neuronal death was assessed by Hoechst 33342 staining. Flow cytometry was used to determine the apoptotie 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 pM 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 （10μM） for 24 h attenuated the damaging effect of Aβ25-5 on the cell viability, and the percentage of apoptotic cells was decreased to 22.62%. Moreover, the increase of ROS induced by Aβ25-5 was inhibited by xylocoside G （10μM）. 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.
