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口服锦葵素在 6-羟多巴胺诱导的半帕金森大鼠模型中具有剂量依赖性的神经保护作用。

Oral pelargonidin exerts dose-dependent neuroprotection in 6-hydroxydopamine rat model of hemi-parkinsonism.

机构信息

Department of Physiology, School of Medicine, Shahed University and Medicinal Plant Research Center, Tehran, Iran.

出版信息

Brain Res Bull. 2010 Jul 30;82(5-6):279-83. doi: 10.1016/j.brainresbull.2010.06.004. Epub 2010 Jun 15.

Abstract

Parkinson's disease (PD) is a neuropathological and debilitating disorder involving the degeneration of mesencephalic dopaminergic neurons. Neuroprotective effect of pelargonidin (Pel) has already been reported, therefore, this study examined whether Pel administration would attenuate behavioural and structural abnormalities and markers of oxidative stress in an experimental model of PD in rat. For this purpose, unilateral intrastriatal 6-hydroxydopamine (6-OHDA, 12.5mug/5mul of saline-ascorbate)-lesioned rats were pre-treated p.o. with Pel (10 and/or 20mg/kg). Pel administration dose-dependently attenuated the rotational behavior in lesioned rats and protected the neurons of SNC against 6-OHDA toxicity. In addition, pre-treatment with Pel (20mg/kg) significantly decreased the 6-OHDA-induced thiobarbituric acid reactive substances (TBARS) formation, indicative of a neuroprotection against lipid peroxidation. Furthermore, the increase of nitrite levels induced by 6-OHDA, indicate the nitric oxide formation and free radicals production and the decrease of antioxidant defense enzyme superoxide dismutase (SOD) was non-significantly prevented by Pel (20mg/kg). In summary, Pel administration has a dose-dependent neuroprotective effect against 6-OHDA toxicity, partly through attenuating oxidative stress. Our findings suggest that pelargonidin could provide benefits, along with other therapies, in neurodegenerative disorders including PD.

摘要

帕金森病(PD)是一种涉及中脑多巴胺能神经元退化的神经病理学和衰弱性疾病。已经有报道表明矢车菊素(Pel)具有神经保护作用,因此,本研究检查了 Pel 给药是否会减轻 PD 大鼠实验模型中的行为和结构异常以及氧化应激标志物。为此,将单侧纹状体 6-羟多巴胺(6-OHDA,12.5mug/5mul 生理盐水-抗坏血酸)损伤的大鼠进行 Pel(10 和/或 20mg/kg)的口服预处理。Pel 给药剂量依赖性地减轻了损伤大鼠的旋转行为,并保护 SNC 神经元免受 6-OHDA 毒性的侵害。此外,Pel(20mg/kg)预处理可显著降低 6-OHDA 诱导的硫代巴比妥酸反应物质(TBARS)形成,表明对脂质过氧化具有神经保护作用。此外,6-OHDA 诱导的亚硝酸盐水平升高表明一氧化氮形成和自由基产生,而 Pel(20mg/kg)可非显著地防止抗氧化防御酶超氧化物歧化酶(SOD)的减少。总之,Pel 给药对 6-OHDA 毒性具有剂量依赖性的神经保护作用,部分通过减轻氧化应激。我们的研究结果表明,矢车菊素可能会在包括 PD 在内的神经退行性疾病的其他治疗方法中提供益处。

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