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软枣猕猴桃对 MPTP 诱导的帕金森病模型小鼠的保护作用。

Protective effect of Actinidia arguta in MPTP-induced Parkinson's disease model mice.

机构信息

College of Pharmacy, Kinjo Gakuin University, 2-1723 Omori, Moriyama-ku, Nagoya, 463-8521, Japan.

College of Pharmacy, Kinjo Gakuin University, 2-1723 Omori, Moriyama-ku, Nagoya, 463-8521, Japan.

出版信息

Biochem Biophys Res Commun. 2021 May 28;555:154-159. doi: 10.1016/j.bbrc.2021.03.116. Epub 2021 Apr 2.

DOI:10.1016/j.bbrc.2021.03.116
PMID:33819745
Abstract

Parkinson's disease (PD) is a neurodegenerative disease characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra. Oxidative stress-induced neuronal death has been identified as one of the major causes of nigrostriatal degeneration in PD. The fruit of Actinidia arguta (A. arguta), known as sarunashi in Japan, has been reported to show beneficial health effects such as antioxidant, anti-inflammatory, anti-mutagenic, and anticholinergic effects. In this study, we investigated the neuroprotective effects of A. arguta in 1-methyl-4-phenyl-1,2,3,6-tetrahydropypridine (MPTP)-induced PD model mice. A. arguta juice was administered to 7-week-old C57BL/6J mice continuously for 10 days before the first MPTP injection. The degeneration of dopaminergic neurons in the substantia nigra was induced by MPTP (30 mg/kg, i. p.) once daily for five consecutive days. We found that the administration of A. arguta ameliorated MPTP-induced motor impairment and suppressed the MPTP-induced reductions of tyrosine hydroxylase-positive neurons and tyrosine hydroxylase protein expression in the substantia nigra. Our findings suggest that taking A. arguta could provide neuroprotection that delays or prevents the neurodegenerative process of PD.

摘要

帕金森病(PD)是一种神经退行性疾病,其特征是黑质中多巴胺能神经元的进行性退化。氧化应激诱导的神经元死亡已被确定为 PD 中黑质纹状体退化的主要原因之一。猕猴桃(A. arguta)的果实,在日本被称为 sarunashi,据报道具有有益的健康作用,如抗氧化、抗炎、抗突变和抗胆堿能作用。在这项研究中,我们研究了猕猴桃对 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的 PD 模型小鼠的神经保护作用。在第一次 MPTP 注射前,连续 10 天给 7 周龄 C57BL/6J 小鼠灌胃猕猴桃汁。通过每日一次腹腔注射 MPTP(30mg/kg)连续 5 天诱导黑质多巴胺能神经元的退化。我们发现,猕猴桃的给药改善了 MPTP 诱导的运动障碍,并抑制了 MPTP 诱导的黑质中酪氨酸羟化酶阳性神经元和酪氨酸羟化酶蛋白表达的减少。我们的研究结果表明,服用猕猴桃可能提供神经保护作用,延缓或预防 PD 的神经退行性过程。

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