Neuroprotective and Therapeutic Effect of Caffeine on the Rat Model of Parkinson's Disease Induced by Rotenone
Neuroprotective and Therapeutic Effect of Caffeine on the Rat Model of Parkinson's Disease Induced by Rotenone
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DOI：
10.1080/19390211.2016.1275916
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发表时间：
2017-01-01
影响因子：
2.5
通讯作者：
Hosny, Eman N.
中科院分区：
文献类型：
--
作者：
Khadrawy, Yasser A.;Salem, Ahmed M.;Hosny, Eman N.
本研究旨在探讨咖啡因对鱼藤酮诱导的大鼠帕金森病（PD）模型的保护和治疗作用。将大鼠分为鱼藤酮诱导的PD模型（1.5 mg/kg腹腔注射，持续45 d）、保护组（30 mg/kg腹腔注射）和鱼藤酮45 d （PD模型建立期间）、治疗组（30 mg/kg腹腔注射，持续45 d）。PD动物模型中脑和纹状体处于氧化应激和亚硝化应激状态，脂质过氧化和一氧化氮水平升高，还原型谷胱甘肽水平降低，s -谷胱甘肽转移酶和超氧化物歧化酶活性降低。鱼藤酮诱导大鼠中脑和纹状体乙酰胆碱酯酶和Na+/K(+-) atp酶活性降低，肿瘤坏死因子-a水平升高。咖啡因保护和处理可改善鱼藤酮诱导的大鼠中脑和纹状体氧化应激及乙酰胆碱酯酶和Na+/K+- atp酶活性的变化。这与PD模型中两个区域的组织病理学改变的改善有关。咖啡因保护和治疗恢复了鱼藤酮引起的中脑和纹状体多巴胺的消耗，防止了运动活动（通过开放场试验评估）和肌肉力量（通过牵引和悬挂试验评估）的下降，并提高了这两个区域的去甲肾上腺素水平。本研究表明，咖啡因对鱼藤酮诱导的帕金森大鼠模型的神经化学、组织病理学和行为改变具有显著的神经保护和治疗作用。
The present study aimed to investigate the protective and therapeutic effects of caffeine on rotenone-induced rat model of Parkinson's disease (PD). Ratswere divided into control, PD model induced by rotenone (1.5 mg/kg intraperitoneally (i.p.) for 45 days), protected group injected with caffeine (30 mg/kg, i.p.) and rotenone for 45 days (during the development of PD model), and treated group injected with caffeine (30 mg/kg, i.p.) for 45 days after induction of PD model. The data revealed a state of oxidative and nitrosative stress in the midbrain and the striatum of animal model of PD as indicated from the increased lipid peroxidation and nitric oxide levels and the decreased reduced glutathione level and activities of glutathione-S-transferase and superoxide dismutase. Rotenone induced a decrease in acetylcholinesterase and Na+/K(+-)ATPase activities and an increase in tumor necrosis factor-a level in the midbrain and the striatum. Protection and treatment with caffeine ameliorated the oxidative stress and the changes in acetylcholinesterase and Na+/K+-ATPase activities induced by rotenone in the midbrain and the striatum. This was associated with improvement in the histopathological changes induced in the two areas of PD model. Caffeine protection and treatment restored the depletion of midbrain and striatal dopamine induced by rotenone and prevented decline in motor activities (assessed by open field test) and muscular strength (assessed by traction and hanging tests) and improved norepinephrine level in the two areas. The present study showed that caffeine offered a significant neuroprotection and treatment against neurochemical, histopathological, and behavioral changes in a rotenone-induced rat model of PD.