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黑种草生物活性化合物百里醌在6-羟基多巴胺诱导的半侧帕金森病大鼠模型中的神经保护作用。

Neuroprotective effect of thymoquinone, the nigella sativa bioactive compound, in 6-hydroxydopamine-induced hemi-parkinsonian rat model.

作者信息

Sedaghat Reza, Roghani Mehrdad, Khalili Mohsen

机构信息

Department of Pathology and Anatomy, School of Medicine, Shahed University, Tehran, Iran.

Neurophysiology Research Center, Shahed University, Tehran, Iran.

出版信息

Iran J Pharm Res. 2014 Winter;13(1):227-34.

PMID:24734075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3985249/
Abstract

Parkinson disease (PD) is the most common movement disorder with progressive degeneration of midbrain dopaminergic neurons for which current treatments afford symptomatic relief with no-prevention of disease progression. Due to the neuroprotective property of the Nigella sativa bioactive compound thymoquinone (TQ), this study was undertaken to evaluate whether TQ could improve behavioral and cellular abnormalities and markers of oxidative stress in an experimental model of early PD in rat. Unilateral intrastriatal 6-hydroxydopamine (6-OHDA)-lesioned rats were daily pretreated p.o. with TQ at doses of 5 and/or 10 mg/Kg three times at an interval of 24 h. After 1 week, apomorphine caused contralateral rotations, a reduction in the number of neurons on the left side of the substantia nigra pars compacta (SNC) was observed, malondialdehyde (MDA) and nitrite level in midbrain homogenate increased and activity of superoxide dismutase (SOD) reduced in the 6-OHDA lesion group. TQ pretreatment significantly improved turning behavior, prevented loss of SNC neurons, and lowered level of MDA. These results suggest that TQ could afford neuroprotection against 6-OHDA neurotoxicity that is partly due to the attenuation of lipid peroxidation and this may provide benefits, along with other therapies, in neurodegenerative disorders including PD.

摘要

帕金森病(PD)是最常见的运动障碍性疾病,其特征为中脑多巴胺能神经元进行性退化,目前的治疗方法只能缓解症状,无法阻止疾病进展。由于黑种草生物活性化合物百里醌(TQ)具有神经保护特性,本研究旨在评估TQ是否能改善大鼠早期PD实验模型中的行为和细胞异常以及氧化应激标志物。对单侧纹状体内注射6-羟基多巴胺(6-OHDA)损伤的大鼠,每天口服给予剂量为5和/或10 mg/Kg的TQ,间隔24小时给药三次。1周后,阿扑吗啡引起对侧旋转,观察到黑质致密部(SNC)左侧神经元数量减少,6-OHDA损伤组中脑匀浆丙二醛(MDA)和亚硝酸盐水平升高,超氧化物歧化酶(SOD)活性降低。TQ预处理显著改善了旋转行为,防止了SNC神经元的丢失,并降低了MDA水平。这些结果表明,TQ可以提供针对6-OHDA神经毒性的神经保护作用,这部分归因于脂质过氧化的减弱,并且这可能与其他疗法一起,在包括PD在内的神经退行性疾病中带来益处。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baa3/3985249/bab374a47763/ijpr-13-227-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baa3/3985249/b166da5ddbe4/ijpr-13-227-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baa3/3985249/276833694d7c/ijpr-13-227-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baa3/3985249/905de34e16d3/ijpr-13-227-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baa3/3985249/bab374a47763/ijpr-13-227-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baa3/3985249/b166da5ddbe4/ijpr-13-227-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baa3/3985249/276833694d7c/ijpr-13-227-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baa3/3985249/905de34e16d3/ijpr-13-227-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baa3/3985249/bab374a47763/ijpr-13-227-g004.jpg

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