南岭柞木苷G对Aβ25-35诱导的PC12细胞损伤的保护作用

南岭柞木苷G对Aβ_25-35诱导的PC12细胞损伤的保护作用

葛嘉, 于艳, 崔德华^*, 屠鹏飞^*

1. 北京大学天然药物及仿生药物国家重点实验室, 北京 100191

2. 北京大学神经科学研究所, 北京 100191

收稿日期:2008-10-08 修回日期:2009-02-10 出版日期:2009-03-15 发布日期:2009-03-15
通讯作者: 崔德华*, 屠鹏飞*

Protective effect of xylocoside G on Aβ_25-35-induced neurotoxicity in PC12 cells

Jia Ge, Yan Yu, De-Hua Cui^*, Peng-Fei Tu^*

1. The State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China

2. Neuroscience Research Institute and Department of Neurobiology; Key Laboratory for Neuroscience Ministry of Education; Key Laboratory for Neuroscience Ministry of Public Health, Peking University, Beijing 100191, China

Received:2008-10-08 Revised:2009-02-10 Online:2009-03-15 Published:2009-03-15
Contact: De-Hua Cui*, Peng-Fei Tu*

摘要/Abstract

摘要：

研究南岭柞木苷G对β淀粉样蛋白25-35片断(Aβ25-35)诱导的PC12细胞损伤的保护作用。用25 μM聚集状的Aβ25-35建立神经细胞损伤模型, 将培养的PC12细胞分为空白对照组, Aβ25-35模型组, Aβ25-35+药物组, 采用MTT比色法, Hoechst 33342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) 25 μM聚集状的Aβ25-35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Aβ25-35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Aβ25-35引起的细胞内活性氧的产生。南岭柞木苷G能抑制Aβ25-35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。

关键词: 南岭柞木苷G, 淀粉样蛋白25-35, 细胞凋亡, 活性氧

Abstract:

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 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 Aβ25-35on the cell viability, and the percentage of apoptotic cells was decreased to 22.62%. Moreover, the increase of ROS induced by Aβ25-35was 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.

Key words: Xylocoside G, Xylocoside G, Aβ25-35, Aβ25-35, Apoptosis, Apoptosis, Reactive oxygen species, Reactive oxygen species

中图分类号:

R285.5

Supporting: Foundation items: Changjiang Scholar and Innovative Team in University (Grant No. 985-2-063-112), National Natural Science Foundation of China (Grant No. 30570533 and 30670414) and China 973 Project (Grant No. 2006CB500705).
^*Corresponding author. Tel.: 86-10-82801702

葛嘉, 于艳, 崔德华^*, 屠鹏飞^*

南岭柞木苷G对Aβ_25-35诱导的PC12细胞损伤的保护作用

[J]. .

Jia Ge, Yan Yu, De-Hua Cui^*, Peng-Fei Tu^*

Protective effect of xylocoside G on Aβ_25-35-induced neurotoxicity in PC12 cells

[J]. .

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