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生酮饮食对 MPTP 诱导的神经毒性的神经保护和抗炎作用。

Neuroprotective and anti-inflammatory activities of ketogenic diet on MPTP-induced neurotoxicity.

机构信息

Department of Human Anatomy, Jining Medical College, 45 Jianshe Nanlu, Jining City, Shandong Province, People's Republic of China.

出版信息

J Mol Neurosci. 2010 Oct;42(2):145-53. doi: 10.1007/s12031-010-9336-y. Epub 2010 Mar 24.

Abstract

Ketogenic diet (KD) is a high-fat, low-protein and low-carbohydrate diet. It is reported that KD can provide the neuroprotection for the neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease (PD) and amyotrophic lateral sclerosis. The main clinical symptom of PD is motor dysfunction derived from the loss of dopaminergic neurons in the substantia nigra (SN) and dopamine content in the striatum subsequently. It is well known that treatments with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mice produce motor dysfunction, biochemical, and neurochemical changes remarkably similar to idiopathic PD patients. In this study, we investigated the neuroprotective and anti-inflammatory effects of KD in MPTP-treated mice. The data showed that pretreatment with KD alleviated the motor dysfunction induced by MPTP. The decrease of Nissl-staining and tyrosine hydroxylase (TH)-positive neurons induced by MPTP was inhibited in the SN. The change of dopamine was very similar to dopaminergic neurons in the SN. KD inhibited the activation of microglia induced by MPTP in the SN. The levels of proinflammatory cytokines (interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha) in the SN were also decreased and induced by MPTP. So, we concluded that KD was neuroprotective and anti-inflammatory against MPTP-neurotoxicity.

摘要

生酮饮食(KD)是一种高脂肪、低蛋白质和低碳水化合物的饮食。据报道,KD 可以为神经退行性疾病(如阿尔茨海默病、帕金森病(PD)和肌萎缩侧索硬化症)提供神经保护。PD 的主要临床症状是源于黑质(SN)中多巴胺能神经元丧失和纹状体中多巴胺含量随后下降的运动功能障碍。众所周知,在小鼠中使用 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)治疗会产生与特发性 PD 患者非常相似的运动功能障碍、生化和神经化学变化。在这项研究中,我们研究了 KD 在 MPTP 处理的小鼠中的神经保护和抗炎作用。数据表明,KD 预处理减轻了 MPTP 引起的运动功能障碍。MPTP 诱导的 SN 中尼氏染色和酪氨酸羟化酶(TH)阳性神经元减少得到抑制。多巴胺的变化与 SN 中的多巴胺能神经元非常相似。KD 抑制了 MPTP 在 SN 中诱导的小胶质细胞激活。MPTP 诱导的 SN 中促炎细胞因子(白细胞介素-1β、白细胞介素-6 和肿瘤坏死因子-α)的水平也降低。因此,我们得出结论,KD 对 MPTP 神经毒性具有神经保护和抗炎作用。

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