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首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >Acetyl-L-carnitine protects dopaminergic nigrostriatal pathway in 6-hydroxydopamine-induced model of Parkinson's disease in the rat
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Acetyl-L-carnitine protects dopaminergic nigrostriatal pathway in 6-hydroxydopamine-induced model of Parkinson's disease in the rat

机译：乙酰-1-肉碱在大鼠帕金森病诱导的6-羟基羟胺诱导的帕金森病模型中保护多巴胺能达曲线途径

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摘要

Parkinson's disease (PD) is a movement disorder and the second most common neurodegenerative disease worldwide in which nigrostriatal dopaminergic neurons within substantia nigra pars compacta (SNC) are lost, with clinical motor and non-motor symptoms including bradykinesia, resting tremor, rigidity, stooping posture and cognitive deficits. This study was undertaken to evaluate the neuroprotective potential of acetyl-L-carnitine (ALC) against unilateral striatal 6-hydroxydopamine (6-OHDA)-induced model of PD and to explore some involved mechanisms. In this experimental study, intrastriatal 6-OHDA-lesioned rats received ALC at doses of 100 or 200 mg/kg/day for 1 week. ALC (200 mg/kg) lowered apomorphine-induced rotational asymmetry and reduced the latency to initiate and the total time in the narrow beam test, reduced striatal malondialdehyde (MDA), increased catalase activity and glutathione (GSH) level, prevented reduction of nigral tyrosine hydroxylase (TH)-positive neurons and striatal TH-immunoreactivity, and lowered striatal glial fibrillary acidic protein (GFAP) and its immunoreactivity as an indicator of astrogliosis, and nuclear factor NF-kappa B and Toll-like receptor 4 (TLR4) as reliable markers of neuroinflammation. Meanwhile, ALC at both doses mitigated nigral DNA fragmentation as a valuable marker of apoptosis. The results of this study clearly suggest the neuroprotective effect of ALC in 6-OHDA-induced model of PD through abrogation of neuroinflammation, apoptosis, astrogliosis, and oxidative stress and it may be put forward as an ancillary therapeutic candidate for controlling PD. (C) 2017 Elsevier Masson SAS. All rights reserved.
机译：帕金森病（PD）是一种运动障碍和全球性的第二种最常见的神经变性疾病，其中患者内吉拉氏菌菌在体积内容中的尼格松多巴胺能神经元（SNC）丧失，临床电机和非运动症状，包括Bradykinesia，休息震颤，刚性，僵硬姿势和认知赤字。本研究旨在评估乙酰-1-肉碱（ALC）对单侧纹状体6-羟基多胺（6-OHDA）诱导的PD模型的神经保护潜力，并探讨一些涉及的机制。在该实验研究中，卵巢6-OHDA损伤的大鼠在100或200mg / kg /天的剂量为1周的剂量下接受ALC。 ALC（200mg / kg）降低仲孔诱导的旋转不对称性，并降低了延迟的启动和窄光束试验中的总时间，减少纹缘丙二醛（MDA），增加的过氧化氢酶活性和谷胱甘肽（GSH）水平，预防八峰减少酪氨酸羟化酶（Th） - 阳性神经元和纹纹纤维纤维酸性蛋白（GFAP）及其免疫反应性，作为星形射精指标，核因子NF-Kappa B和Toll样受体4（TLR4）作为神经引发的可靠标记。同时，两种剂量的ALC减轻了八藻DNA碎片作为细胞凋亡的有价值标记。该研究的结果清楚地表明ALC在6-OHDA诱导的PD模型中的神经保护作用通过神经炎症，细胞凋亡，星分泌症和氧化应激的脱模，并且可以作为控制PD的辅助治疗候选者提出。 （c）2017年Elsevier Masson SAS。版权所有。

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