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橄榄(Olea europaea L.)叶的水醇提取物对鱼藤酮诱导的大鼠帕金森病的神经保护作用。

The neuroprotective effects of hydro-alcoholic extract of olive (Olea europaea L.) leaf on rotenone-induced Parkinson's disease in rat.

机构信息

Cellular and Molecular Research Center, Zahedan University of Medical Sciences, Zahedan, IR, Iran.

Department of Anatomy, School of Medicine, Zahedan University of Medical Sciences, Zahedan, IR, Iran.

出版信息

Metab Brain Dis. 2018 Feb;33(1):79-88. doi: 10.1007/s11011-017-0131-0. Epub 2017 Oct 16.

Abstract

Parkinson's disease (PD) is an age-related disease in which dopaminergic neurons in the nigrostriatal pathway are destroyed, resulting in movement and behavioral problems. Oxidative stress and the generation of reactive oxygen species play key roles in neurodegenerative diseases, such as PD. Rotenone (ROT) is a common pesticide that induces oxidative stress. Olive leaves extract (OLE) has antioxidant and neuroprotective effects. Thus, the aim of this study was to investigate the neuroprotective effects of OLE on ROT-induced oxidative stress in the midbrain of a rat model of PD. Ninety-six Wistar rats were randomly divided into the following 6 groups (n = 16 rats/group): Control, Sham, ROT, and 3 ROT + OLE (75, 150, and 300 mg/kg/daily) groups. ROT (2.5 mg/kg/48 h) was injected subcutaneously, and vehicle or OLE was orally administered for 30 days. The animals were then sacrificed, and their brains were removed. Biochemical measures, including the levels of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA), and the number of tyrosine hydroxylase (TH)-positive neurons were determined, and behavioral (rotarod and hanging) tests were conducted. The balance and muscle strength of the OLE (150 and 300 mg/kg)-treated groups were significantly improved. Treatment with OLE prevented the increases in the levels of MDA, significantly improved the SOD, CAT, and GPx levels in the midbrain, and prevented the depletion of the TH-positive neurons. These findings suggested that OLE has neuroprotective properties and that it might be useful for preventing the death of dopaminergic neurons in patients with PD.

摘要

帕金森病(PD)是一种与年龄相关的疾病,其中黑质纹状体通路中的多巴胺能神经元被破坏,导致运动和行为问题。氧化应激和活性氧的产生在神经退行性疾病中起关键作用,如 PD。鱼藤酮(ROT)是一种常见的杀虫剂,可诱导氧化应激。橄榄油提取物(OLE)具有抗氧化和神经保护作用。因此,本研究旨在探讨 OLE 对 PD 大鼠模型中 ROT 诱导的中脑氧化应激的神经保护作用。96 只 Wistar 大鼠随机分为以下 6 组(n = 16 只/组):对照组、假手术组、ROT 组和 3 个 ROT + OLE(75、150 和 300 mg/kg/天)组。ROT(2.5 mg/kg/48 h)皮下注射,载体或 OLE 口服给药 30 天。然后处死动物,取出大脑。测定生化指标,包括过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)和丙二醛(MDA)水平,以及酪氨酸羟化酶(TH)阳性神经元数量,并进行行为(旋转和悬挂)测试。OLE(150 和 300 mg/kg)治疗组的平衡和肌肉力量明显改善。OLE 治疗可防止 MDA 水平升高,显著改善中脑 SOD、CAT 和 GPx 水平,并防止 TH 阳性神经元耗竭。这些发现表明 OLE 具有神经保护特性,可能有助于预防 PD 患者多巴胺能神经元的死亡。

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