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培养神经细胞的氧自由基损伤及银杏叶提取物的治疗作用
引用本文:杨玲玲,苑辉卿,曾季平,郝建荣,胡晓燕,崔行. 培养神经细胞的氧自由基损伤及银杏叶提取物的治疗作用[J]. 中国老年学杂志, 2005, 25(1): 56-58
作者姓名:杨玲玲  苑辉卿  曾季平  郝建荣  胡晓燕  崔行
作者单位:山东大学医学院生物化学与分子生物学研究所,山东,济南,250012
基金项目:山东省卫生厅九五攻关课题
摘    要:目的 探讨氧自由基在Alzheimer病(AD)发病中的作用和评价银杏叶提取物(Ginkgo biloba extract,EGb)的临床应用价值。方法 以产生超氧阴离子系统黄嘌呤/黄嘌呤氧化酶(X/XO)作用于PC12细胞,并以EGb拮抗其作用,电镜观察细胞形态变化,MTF法检测细胞存活率,流式细胞术分析细胞凋亡情况,RT-PCR技术分析凋亡相关基因Bcl-2、Bax表达变化。结果 经X/XO损伤后,细胞存活率降低,凋亡率增加,促凋亡基因Bax表达上调。EGb(20mg/L)能改善凋亡情况。结论氧 自由基可诱导神经细胞凋亡而促进AD发生,EGb对神经细胞有保护作用,提示可用于AD的临床治疗与预防.

关 键 词:活性氧 阿尔茨海默病 细胞凋亡 凋亡相关基因
文章编号:1005-9202(2005)01-0056-03
修稿时间:2004-05-10

Reactive oxygen species-induced cultured neurons apoptosis and the therapeutic effect of EGb
YANG Ling-ling,YUAN Hui-qing,ZENG Ji-ping,et al.. Reactive oxygen species-induced cultured neurons apoptosis and the therapeutic effect of EGb[J]. Chinese Journal of Gerontology, 2005, 25(1): 56-58
Authors:YANG Ling-ling  YUAN Hui-qing  ZENG Ji-ping  et al.
Affiliation:YANG Ling-ling,YUAN Hui-qing,ZENG Ji-ping,et al .
Abstract:Objective To explore the toxic effects of reactive oxygen species (ROS) in Alzheimer's disease (AD) and the therapeutic value of ginkgo biloba extract (EGb). Methods The authors exposed PC12 cells to X/XO and used the EGb to resist the effect, then observed the changes of cells under electron microscope, measured the cell survival rate by MTT assay and analyzed the apoptosis of cells with flow cytometric analysis. The expression change of apoptosis-associated gene (AAG) bax and bcl-2 were detected by RT-PCR. Results Exposure of cells to X/XO resulted in decrease of cell survival rate and increase of the apoptosis rate, as well as an elevation of bax expression. EGb (20 mg/L) could ameliorate the apoptosis. Conclusions ROS can induce neurons apoptosis, which may play important role in the progress of AD. EGb can protect neurons against ROS-induced apoptosis, so it also can be used for AD's therapy and prevention.
Keywords:Reactive oxygen species (ROS)  Alzheimer's disease (AD)  Cellular apoptosis  Apoptosis associated gene
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