Xu Qi, Langley Monica, Kanthasamy Anumantha G, Reddy Manju B
Departments of Food Science and Human Nutrition and.
School of Public Health, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
J Nutr. 2017 Oct;147(10):1926-1931. doi: 10.3945/jn.117.255034. Epub 2017 Aug 23.
Parkinson disease (PD) is a neurodegenerative disorder that has been associated with many factors, including oxidative stress, inflammation, and iron accumulation. The antioxidant, anti-inflammatory, and iron-chelating properties of epigallocatechin gallate (EGCG), a major polyphenol in green tea, may offer protection against PD. We sought to determine the neurorescue effects of EGCG and the role of iron in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. We evaluated the neurorescue effect of EGCG (25 mg/kg, 7 d, oral administration) against MPTP-induced (20 mg/kg, 3 d, intraperitoneal injection) neurodegeneration in C57 male black mice. Thirty mice weighing ∼25 g were divided into 3 groups: control, MPTP, and MPTP + EGCG. The neurorescue effect of EGCG was assessed with the use of motor behavior tests, neurotransmitter analysis, oxidative stress indicators, and iron-related protein expression. Compared with the control group, MPTP treatment shortened the mice's latency to fall from the rotarod by 16% ( < 0.05), decreased the striatal dopamine concentration by 58% ( < 0.001) and dihydroxyphenylacetic acid by 35% ( < 0.05), and increased serum protein carbonyls by 71% ( = 0.07). However, EGCG rescued MPTP-induced neurotoxicity by increasing the rotational latency by 17% ( < 0.05) to a value similar to the control group. Striatal dopamine concentrations were 40% higher in the MPTP + EGCG group than in the MPTP group ( < 0.05), but the values were significantly lower than in the control group. Compared with the MPTP and control groups, mice in the MPTP + EGCG group had higher substantia nigra ferroportin expression (44% and 35%, respectively) ( < 0.05) but not hepcidin and divalent metal transporter 1 expression. Overall, our study demonstrated that EGCG regulated the iron-export protein ferroportin in substantia nigra, reduced oxidative stress, and exerted a neurorescue effect against MPTP-induced functional and neurochemical deficits in mice.
帕金森病（PD）是一种神经退行性疾病，与多种因素相关，包括氧化应激、炎症和铁蓄积。表没食子儿茶素没食子酸酯（EGCG）是绿茶中的一种主要多酚，其抗氧化、抗炎和铁螯合特性可能对帕金森病起到保护作用。我们试图确定EGCG的神经保护作用以及铁在1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的帕金森病中的作用。我们评估了EGCG（25毫克/千克，7天，口服给药）对C57雄性黑小鼠中MPTP诱导（20毫克/千克，3天，腹腔注射）的神经退行性变的神经保护作用。30只体重约25克的小鼠被分为3组：对照组、MPTP组和MPTP + EGCG组。通过运动行为测试、神经递质分析、氧化应激指标和铁相关蛋白表达来评估EGCG的神经保护作用。与对照组相比，MPTP处理使小鼠从转棒上掉落的潜伏期缩短了16%（P < 0.05），纹状体多巴胺浓度降低了58%（P < 0.001），二羟基苯乙酸降低了35%（P < 0.05），血清蛋白羰基增加了71%（P = 0.07）。然而，EGCG通过将旋转潜伏期增加17%（P < 0.05），使其恢复到与对照组相似的值，从而挽救了MPTP诱导的神经毒性。MPTP + EGCG组的纹状体多巴胺浓度比MPTP组高40%（P < 0.05），但该值显著低于对照组。与MPTP组和对照组相比，MPTP + EGCG组小鼠黑质铁转运蛋白表达更高（分别为44%和35%）（P < 0.05），但铁调素和二价金属转运蛋白1表达无变化。总体而言，我们的研究表明，EGCG调节黑质中铁输出蛋白铁转运蛋白，降低氧化应激，并对MPTP诱导的小鼠功能和神经化学缺陷发挥神经保护作用。
