Abstract：
Parkinson\'s disease (PD) affects about 8.5 million individuals worldwide. Oxidative and inflammatory cascades are implicated in the neurological sequels, that are mostly unresolved in PD treatments. However, proper nutrition offers one of the most effective and least costly ways to decrease the burden of many diseases and their associated risk factors. Moreover, prevention may be the best response to the progressive nature of PD, thus, the therapeutic novelty of honey and levodopa may be prospective. This study aimed to investigate the neuroprotective role of honey and levodopa against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced oxidative stress. Fifty-four adult male Swiss mice were divided into control and PD model groups of 27 mice. Each third of the control mice either received phosphate buffered saline, honey, or levodopa for 21 days. However, each third of the PD models was either pretreated with honey and levodopa or not pretreated. Behavioral studies and euthanasia were conducted 2 and 8 days after MPTP administration respectively. The result showed that there were significantly (P<0.05) higher motor activities in the PD models pretreated with the honey as well as levodopa. furthermore, the pretreatments protected the midbrain against the chromatolysis and astrogliosis induced by MPTP. The expression of antioxidant markers (glutathione [GSH] and nuclear factor erythroid 2-related factor 2 [Nrf2]) was also significantly upregulated in the pretreated PD models. It is thus concluded that honey and levodopa comparably protected the substantia nigra pars compacta neurons against oxidative stress by modulating the Nrf2 signaling molecule thereby increasing GSH level to prevent MPTP-induced oxidative stress.
摘要：
帕金森病（PD）影响全球约850万人。氧化和炎症级联反应与神经后遗症有关，在PD治疗中大多未解决。然而,适当的营养为减轻许多疾病及其相关危险因素的负担提供了最有效和最便宜的方法之一。此外，预防可能是对PD进行性的最佳反应，因此，蜂蜜和左旋多巴的治疗新颖性可能是有前景的。本研究旨在研究蜂蜜和左旋多巴对1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的氧化应激的神经保护作用。将54只成年雄性瑞士小鼠分为27只小鼠的对照和PD模型组。每三分之一的对照小鼠接受磷酸盐缓冲盐水，蜂蜜,或左旋多巴21天。然而,每三分之一的PD模型使用蜂蜜和左旋多巴预处理或未预处理.分别在MPTP给药后2天和8天进行行为研究和安乐死。结果表明，用蜂蜜和左旋多巴预处理的PD模型的运动活动显着（P<0.05）。此外，预处理可保护中脑免受MPTP诱导的色谱分解和星形胶质增生。在预处理的PD模型中，抗氧化标记物（谷胱甘肽[GSH]和核因子红系2相关因子2[Nrf2]）的表达也显着上调。因此得出结论，蜂蜜和左旋多巴通过调节Nrf2信号分子从而提高GSH水平以防止MPTP诱导的氧化应激，从而相对地保护黑质致密神经元免受氧化应激。
