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百里醌在帕金森病动物模型中发挥神经保护作用。

Thymoquinone exerts neuroprotective effect in animal model of Parkinson's disease.

作者信息

Ebrahimi Seyedeh Shohreh, Oryan Shahrbanoo, Izadpanah Esmael, Hassanzadeh Kambiz

机构信息

Department of Animal Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran.

Cellular & Molecular Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran; Department of Physiology and Pharmacology, Kurdistan University of Medical Sciences, Sanandaj, Iran.

出版信息

Toxicol Lett. 2017 Jul 5;276:108-114. doi: 10.1016/j.toxlet.2017.05.018. Epub 2017 May 17.

DOI:10.1016/j.toxlet.2017.05.018
PMID:28526446
Abstract

Oxidative stress plays an important role in both the initiation and progression of Parkinson's disease (PD). Rotenone, an environmental toxin, induces oxidative stress and impact mitochondrial dynamics, including fission and fusion. Thymoquinone (TQ) has been reported to have antioxidant and anti-inflammatory characteristics in vitro and in vivo. TQ scavenges free radicals so prevents cell damage against oxidative agents. To evaluate the efficacy of TQ in the management of PD, male Wistar rats (8-10 months) received rotenone. Pre-treatment with TQ (7.5 and 15mg/kg/day, po) one hour prior to the rotenone injection, changed motor tests results (rotarod, rearing and bar tests). Dopamine levels of dopaminergic areas in the substantia nigra (SN) and striatum (ST) measured using high-performance liquid chromatography. Western blot analysis employed to determine the protein contents of Parkin and Drp1 (dynamin-related protein-1) in these areas and in order to identify tyrosine hydroxylase positive cells, Immunohistochemical assays performed. The results indicated that TQ significantly prevented rotenone-induced motor defects and changes in the Parkin, Drp1, dopamine and TH levels in both studied areas. These findings show that TQ effects on ameliorating the PD symptoms induced by rotenone might be associated with the neuroprotective and antioxidant effects of this compound.

摘要

氧化应激在帕金森病(PD)的发生和发展中均起重要作用。鱼藤酮作为一种环境毒素,可诱导氧化应激并影响线粒体动力学,包括裂变和融合。据报道,百里醌(TQ)在体外和体内均具有抗氧化和抗炎特性。TQ可清除自由基,从而防止细胞受到氧化应激剂的损伤。为评估TQ对帕金森病的治疗效果,对8 - 10月龄雄性Wistar大鼠注射鱼藤酮。在注射鱼藤酮前1小时,用TQ(7.5和15mg/kg/天,口服)进行预处理,改变了运动测试结果(转棒试验、竖毛试验和横杆试验)。采用高效液相色谱法测定黑质(SN)和纹状体(ST)中多巴胺能区域的多巴胺水平。通过蛋白质免疫印迹分析来测定这些区域中帕金蛋白和动力相关蛋白1(Drp1)的含量,并且为了鉴定酪氨酸羟化酶阳性细胞,进行了免疫组织化学检测。结果表明,TQ显著预防了鱼藤酮诱导的运动缺陷以及两个研究区域中帕金蛋白、Drp1、多巴胺和酪氨酸羟化酶水平的变化。这些发现表明,TQ对改善鱼藤酮诱导的帕金森病症状的作用可能与其神经保护和抗氧化作用有关。

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