《中国康复理论与实践》

《中国康复理论与实践》 ›› 2010, Vol. 16 ›› Issue (10): 913-915.

• 论文 • 上一篇    下一篇

表没食子儿茶素没食子酸酯对MPTP致多巴胺能神经元损伤的保护作用

王涛1，岳峰1，刘佳1，左萍萍2，陈彪1   

  1. 1.首都医科大学宣武医院神经生物学研究室，教育部神经变性病学重点实验室，北京市 100053；2.中国医学科学院基础医学研究所药理室，北京市 100005。
  • 收稿日期:2010-08-31 修回日期:1900-01-01 出版日期:2010-10-25 发布日期:2010-10-25
  • 通讯作者: 陈彪

Protective Effects of Epigallocatechin Gallate in MPTP-induced Mouse Model of Parkinson's Disease

WANG Tao, YUE Feng, LIU Jia, et al   

  1. Department of Neurobiology, Key Laboratory on Neurodegenerative Disorders of Ministry of Education, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing 100053, China
  • Received:2010-08-31 Revised:1900-01-01 Published:2010-10-25 Online:2010-10-25

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摘要： 目的研究表没食子儿茶素没食子酸酯(EGCG)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)致帕金森病模型小鼠多巴胺能神经元的保护作用。方法32只雄性C57BL/6小鼠随机分为4组：假手术组腹腔注射等量生理盐水，模型组腹腔注射4次MPTP(16 mg/kg，间隔2 h)，EGCG治疗组为MPTP+EGCG(5 mg/kg)组，EGCG正常给药组不做任何处理，每日给予5 mg/kg EGCG。连续给药3周后检测行为学指标，黑质酪氨酸羟化酶(TH)免疫组化染色及高效液相色谱-电化学法测定纹状体内多巴胺及其代谢产物浓度。结果模型组5 min内的自发运动次数(71.4±14.0)下降，而EGCG治疗组自发运动次数(87.9±10.7)提高(P<0.05)。与模型组转杆停留时间(73.5±24.9) s相比，EGCG治疗组转杆停留时间(118.6±31.2) s延长(P<0.05)。形态学结果显示，EGCG治疗组黑质TH阳性神经元与模型组相比，数量明显增多。模型组纹状体内多巴胺(DA)及其代谢产物3,4-双羟苯乙酸(DOPAC)和高香草酸(HVA)浓度显著降低，而EGCG治疗组DA、DOPAC和HVA浓度虽有一定程度升高，但无统计学差异。结论EGCG改善MPTP致帕金森病模型小鼠的运动能力下降，对黑质多巴胺神经元有保护作用。

关键词: 帕金森病, 表没食子儿茶素没食子酸酯, 神经保护, 多巴胺

Abstract: ObjectiveTo investigate the protective effects of epigallocatechin gallate (EGCG) in a mouse model of Parkinson's disease induced by 1-Methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP).Methods32 C57BL/ 6 male mice were randomly divided into 4 groups: Model group was administrated with 16 mg/kg MPTP (i.p., four times, 2 h interval); Sham group was treated with saline; EGCG treatment group was given EGCG (5 mg/kg) after MPTP administration; normal group was just given EGCG (5 mg/kg) as treatment group. After given EGCG for 3 weeks, behavioral tests, tyrosine hydroxylase (TH) immunohistochemistry staining and the HPLC for dopamine (DA) and its metabolites were used.ResultsThe present results indicated that oral administration of EGCG significantly improved the behavioral impairement in mice induced by MPTP (P<0.05). And in the EGCG treatment group, there were more TH-positive neurons than in model group. In addition, levels of DA and its metabolites in striatum decreased significantly in MPTP group (P<0.05). Though the concentration of DA and its metabolites in EGCG treatment group tended to increase, however, there was no significance between EGCG treatment and model group.ConclusionEGCG could improve the behavioral impairment in a mouse model of Parkinson's disease induced by MPTP and protect against the loss of the dopamine neurons in the substantia nigra (SN).

Key words: Parkinson's disease (PD), Epigallocatechin Gallate(EGCG), neuroprotection, dopamine