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表没食子儿茶素没食子酸酯通过抑制小胶质细胞活化来保护多巴胺能神经元免受1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的神经毒性。

Epigallocatechin gallate protects dopaminergic neurons against 1-methyl-4- phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity by inhibiting microglial cell activation.

作者信息

Li Rui, Peng Ning, Du Fang, Li Xu-ping, Le Wei-dong

机构信息

Department of Neurology, People's Hospital of Shaanxi Province, Xi'an 710068, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2006 Apr;26(4):376-80.

Abstract

OBJECTIVE

To observe whether the dopaminergic neuroprotective effect of (-)-epigallocatechin gallate (EGCG) is associated with its inhibition of microglial cell activation in vivo.

METHODS

The effects of EGCG at different doses on dopaminergic neuronal survival were tested in a methyl-4-phenyl-pyridinium (MPP+)-induced dopaminergic neuronal injury model in the primary mesencephalic cell cultures. With unbiased stereological method, tyrosine hydroxylase-immunoreactive (TH-ir) cells were counted in the A8, A9 and A10 regions of the substantia nigra (SN) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated C57BL/6 mice. The effect of EGCG on microglial activation in the SN was also investigated.

RESULTS

Pretreatment with EGCG (1 to 100 micromol/L) significantly attenuated MPP+-induced TH-ir cell loss by 22.2% to 80.5% in the mesencephalic cell cultures. In MPTP-treated C57BL/6 mice, EGCG at a low concentration (1 mg/kg) provided significant protection against MPTP-induced TH-ir cell loss by 50.9% in the whole nigral area and by 71.7% in the A9 region. EGCG at 5 mg/kg showed more prominent protective effect than at 1 or 10 mg/kg. EGCG pretreatment significantly inhibited microglial activation and CD11b expression induced by MPTP.

CONCLUSION

EGCG exerts potent dopaminergic neuroprotective activity by means of microglial inhibition, which shed light on the potential use of EGCG in treatment of Parkinson's disease.

摘要

目的

观察(-)-表没食子儿茶素没食子酸酯(EGCG)的多巴胺能神经保护作用是否与其在体内抑制小胶质细胞活化有关。

方法

在原代中脑细胞培养物中,用甲基-4-苯基吡啶离子(MPP+)诱导的多巴胺能神经元损伤模型测试不同剂量EGCG对多巴胺能神经元存活的影响。采用无偏立体学方法,对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)处理的C57BL/6小鼠黑质(SN)的A8、A9和A10区域中酪氨酸羟化酶免疫反应性(TH-ir)细胞进行计数。还研究了EGCG对SN中小胶质细胞活化的影响。

结果

在中脑细胞培养物中,EGCG(1至100μmol/L)预处理可使MPP+诱导的TH-ir细胞损失显著减少22.2%至80.5%。在MPTP处理的C57BL/6小鼠中,低浓度(1mg/kg)的EGCG可显著保护MPTP诱导的TH-ir细胞损失,在整个黑质区域减少50.9%,在A9区域减少71.7%。5mg/kg的EGCG比1mg/kg或10mg/kg表现出更显著的保护作用。EGCG预处理可显著抑制MPTP诱导的小胶质细胞活化和CD11b表达。

结论

EGCG通过抑制小胶质细胞发挥强大的多巴胺能神经保护活性,这为EGCG在帕金森病治疗中的潜在应用提供了线索。

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