Rahimmi Arman, Khosrobakhsh Farnoosh, Izadpanah Esmael, Moloudi Mohammad Raman, Hassanzadeh Kambiz
Department of Bioscience & Biotechnology, University of Kurdistan, Sanandaj, Iran; Cellular and Molecular Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Department of Bioscience & Biotechnology, University of Kurdistan, Sanandaj, Iran.
Brain Res Bull. 2015 Apr;113:34-40. doi: 10.1016/j.brainresbull.2015.02.007. Epub 2015 Feb 28.
There are convincing evidences that oxidative stress has an important role in both the initiation and progression of Parkinson's disease. N-acetylcysteine (NAC) is shown to have antioxidant properties via fortifying glutathione which is one of the main endogenous antioxidant systems. Therefore our study was aimed to evaluate the effect of NAC in management of Parkinson's disease. To this aim, male Wistar rats (10-12 months) received rotenone 2.5mg/kg/48 h intraperitoneally (ip) to induce a Parkinson's disease model. Pretreatment with NAC (25 and 50mg/kg/48 h ip) was administered 1h before the rotenone injection. Three behavioral tests (rotarod, rearing and bar tests) were performed for motor function assessment. Dopamine levels of dopaminergic areas in rat brain including substantia nigra (SN) and striatum (ST) were assessed using high performance liquid chromatography analysis to measure the loss of dopamine. Western blot analysis was also done for parkin and Drp1 (dynamin related protein-1) proteins quantification in SN and ST. Our results indicated that NAC significantly ameliorated the rotenone-induced motor dysfunction and dopamine loss. Furthermore, NAC was able to prevent the rotenone-induced changes in parkin and Drp1 levels in the both studied areas. In conclusion we found that NAC delayed the Parkinson's disease induction by rotenone and this effect might be related to its proved antioxidant effect.
有令人信服的证据表明，氧化应激在帕金森病的发生和发展中都起着重要作用。N-乙酰半胱氨酸（NAC）通过增强谷胱甘肽（主要内源性抗氧化系统之一）而显示出抗氧化特性。因此，我们的研究旨在评估NAC在帕金森病治疗中的作用。为此，将雄性Wistar大鼠（10 - 12个月）腹腔注射鱼藤酮2.5mg/kg/48h以诱导帕金森病模型。在注射鱼藤酮前1小时给予NAC（25和50mg/kg/48h腹腔注射）进行预处理。进行了三项行为测试（转棒试验、竖毛试验和横杆试验）以评估运动功能。使用高效液相色谱分析法评估大鼠脑内包括黑质（SN）和纹状体（ST）在内的多巴胺能区域的多巴胺水平，以测量多巴胺的损失。还进行了蛋白质印迹分析以定量SN和ST中parkin和Drp1（动力相关蛋白-1）蛋白。我们的结果表明，NAC显著改善了鱼藤酮诱导的运动功能障碍和多巴胺损失。此外，NAC能够防止鱼藤酮诱导的两个研究区域中parkin和Drp水平的变化。总之，我们发现NAC延缓了鱼藤酮诱导的帕金森病，这种作用可能与其已证实的抗氧化作用有关。
