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Nootropic activity of acetaminophen against colchicine induced cognitive impairment in rats

机译:对乙酰氨基酚对秋水仙碱诱导的大鼠认知障碍的促智活性

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摘要

Alzheimer’s disease is a devastating neurodegenerative disorder, the most common among the dementing illnesses. Acetaminophen has gaining importance in neurodegenerative diseases by attenuating the dopaminergic neurodegeneration in Caenorhabditis elegans model, decreasing the chemokines and the cytokines and increasing the anti apoptotic protein such as Bcl-2 in neuronal cell culture. The low concentration acetaminophen improved the facilitation to find the hidden platform in Morris Water Maze Test. Also some data suggest that acetaminophen could contribute in neurodegeneration. The present study was aimed to evaluate the effect of acetaminophen against colchicine induced cognitive impairment and oxidative stress in wistar rats. The cognitive learning and memory behaviour was assessed using step through passive avoidance paradigm and acetylcholine esterase activity. The parameters of oxidative stress were assessed by measuring the malondialdehyde, reduced glutathione and catalase levels in the whole brain homogenates. There was a significant memory improvement in the rats received acetaminophen treatment and it has also decreased the acetylcholine esterase enzyme level, confirming its nootropic activity. Acetaminophen neither increases nor decreases the reduced glutathione and catalase in the whole brain homogenates, showing that acetaminophen is devoid of any adverse effect on brain antioxidant defense system.
机译:阿尔茨海默氏病是毁灭性的神经退行性疾病,是痴呆症中最常见的疾病。对乙酰氨基酚通过减轻秀丽隐杆线虫模型中的多巴胺能神经变性,减少趋化因子和细胞因子并增加神经细胞培养物中的抗凋亡蛋白(如Bcl-2),在神经退行性疾病中具有重要意义。低浓度对乙酰氨基酚改善了在莫里斯水迷宫测试中寻找隐藏平台的便利性。还有一些数据表明对乙酰氨基酚可能会导致神经退行性变。本研究旨在评估对乙酰氨基酚对秋水仙碱诱导的wistar大鼠认知功能损害和氧化应激的影响。使用被动回避范例和乙酰胆碱酯酶活性逐步评估了认知学习和记忆行为。通过测量全脑匀浆中的丙二醛,还原型谷胱甘肽和过氧化氢酶水平来评估氧化应激的参数。在接受对乙酰氨基酚治疗的大鼠中,记忆力显着改善,并且还降低了乙酰胆碱酯酶水平,证实了其促智活性。对乙酰氨基酚在全脑匀浆中既不增加也不减少还原型谷胱甘肽和过氧化氢酶,表明对乙酰氨基酚对脑抗氧化防御系统没有任何不利影响。

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