[1]龚全峰)△,杨红旗).烷丙苯胺对6羟基多巴胺致PC12细胞损伤的改善作用[J].郑州大学学报(医学版),2009,(05):1003-1005.
　GONG Quanfeng),YANG Hongqi).Neuroprotective effects of deprenyl against 6hydroxydopamine inducing neurotoxicity in PC12 cells[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2009,(05):1003-1005.
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烷丙苯胺对6羟基多巴胺致PC12细胞损伤的改善作用()
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《郑州大学学报(医学版)》[ISSN:1671-6825/CN:41-1340/R]

卷:
期数:
2009年05期
页码:
1003-1005
栏目:
论著
出版日期:
2009-09-01

文章信息/Info

Title:
Neuroprotective effects of deprenyl against 6hydroxydopamine inducing neurotoxicity in PC12 cells
作者:
龚全峰1)△; 杨红旗2)
1)郑州市第一人民医院神经内科郑州4500042)河南省人民医院神经内科郑州450003
Author(s):
GONG Quanfeng1);  YANG Hongqi2)
1)Department of Neurology,the First People’s Hospital of Zhengzhou, Zhengzhou 4500042)Department of Neurology, Henan Provincial People’s Hospital, Zhengzhou 450003
关键词:
帕金森病; 烷丙苯胺; 6羟基多巴胺; PC12细胞
Keywords:
Parkinson’s disease;  deprenyl;  6hydroxydopamine; PC12 cell
分类号:
R742.5
摘要:
探讨烷丙苯胺(deprenyl)对多巴胺能神经元的保护作用及其可能机制。方法：将PC12细胞分别暴露于不同浓度的6羟基多巴胺(6OHDA)和deprenyl，用四甲基偶氮唑蓝（MTT）法检测其对细胞活力的影响；Western印迹法检测其对Caspase3表达的影响；荧光法检测deprenyl对6OHDA诱导的Caspase3活性和谷胱甘肽（GSH）活性的影响。结果：1～100μmol/L浓度范围的6OHDA均降低PC12细胞活力（F=23.612,P<0.05），而1～100μmol/L的deprenyl对细胞活力无明显影响(F=0.984,P>0.05)；提前加入1～50μmol/L的deprenyl后可以抵抗50μmol/L的6OHDA对细胞活力的毒性作用（F=26.630,P<0.05）。与对照组相比，6OHDA使Caspase3活性片段释放增加，提前加入deprenyl可以部分拮抗此作用（F=22.151,P<0.05）；与对照组相比，6OHDA降低了GSH的活性，而提前加入deprenyl的可以部分增加GSH的活性（F=8.453，P<0.05）。结论：6OHDA对多巴胺神经元有神经毒性作用，而deprenyl可以部分拮抗6OHDA的毒性作用，deprenyl的神经保护作用可能与抑制Caspase3活性和提高GSH活性有关。
Abstract:
To investigate the neuroprotective effects of deprenyl against 6hydroxydopamine(6OHDA) inducing neurotoxicity in PC12 cells.Methods:Rat PC12 cells were incubated separately with different concentrations of 6OHDA and deprenyl, and their effects on cell viability were measured by MTT assays.The effect of deprenyl on 6OHDAinduced Caspase3 activation was investigated by Western Blot analysis. Then the effects of deprenyl and 6OHDA on Caspase3 and glutathione (GSH) activities were measured.Results: In concentration 1~100 μmol/L, 6OHDA dosedependently decreased cell viability（F=23.612,P<0.05）,while 1～100 μmol/L deprenyl did not significantly decrease cell viability as compared with control group(F=0.984,P>0.05).The decreased cell viability by 50 μmol/L 6OHDA can partially be inhibited by pretreated with 1~50 μmol/L deprenyl（F=26.630,P<0.05）. Western Blot indicated that 6OHDA promoted Caspase3 activation as compared with control group, while this effect was partially antagonized by deprenyl preincubation（F=22.151,P<0.05）.6OHDA decreased GSH activity as compared with control group and this effect was partially blocked by pretreatment with deprenyl(F=8.453，P<0.05).Conclusion: 6OHDA has neurotoxic effects on dopaminergic cells and deprenyl can antagonize the neurotoxic effects of 6OHDA.The neuroprotective effect of deprenyl against 6OHDA may be related with its effect on Caspase3 and GSH activities.

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备注/Memo

备注/Memo:
△男，1966年生，大学本科，副主任医师，研究方向：帕金森病，Email:gong_qf@163.com
更新日期/Last Update: 2010-05-14