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首页> 外文期刊>Journal of biochemical and molecular toxicology >Nootropic effect of neferine on aluminium chloride-induced Alzheimer's disease in experimental models
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Nootropic effect of neferine on aluminium chloride-induced Alzheimer's disease in experimental models

机译：Neferine在实验模型中氯化铝诱导的阿尔茨海默病的垂直效应

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Alzheimer's disease (AD) is an age-associated neurodegenerative disease, which is developed by oxidative stress and acetylcholine contraction in the synaptic cleft of the neurons. This leads to dementia, memory loss, and decrease in learning ability and orientation. In this research work, we aimed to explore the neuroprotective effect of neferine on AICI_3-induced AD in rats. The results of our study revealed that the increased reactive oxygen species (ROS) and nitric oxide in the hippocampus leads to the development of AD in the rats. The oral treatment of neferine done the following occurrences such as; it potentially inhibited the ROS formation and acts as a scavenging molecule by preventing the neurodegenera-tion. It also improved the memory and learning ability to complete the maze activity in the AD rats and significantly increased the antioxidants superoxide dismutase, catalase, and reduced glutathione in neferine treated AD rats. It aggressively declined the activity of acetylcholine esterase and Na~+K~+ATPase in the neurodegenerative rat models. The gene expression pattern of neuroinflam-matory cytokines such as tumor necrosis factor a (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were decreased in the neferine-treated rats. The neuroin-flammatory proteins such as inducible nitric oxide (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor kappa β (Nf-κβ) were decreased and Nf-κβ inhibitor IKBα was increased in the neferine-treated AD rats. Finally, the histology study proved that the neferine treatment possibly prevents neurodegeneration in the hippocampus tissue of the AD models. Hence, these all findings concluded that the neferine could be a potential neuropreventive as well as neurodegenerative therapeutic compound in neurological and cognitive dysfunction.
机译：阿尔茨海默病（Alzheimer’s disease，AD）是一种与年龄相关的神经退行性疾病，由神经元突触间隙的氧化应激和乙酰胆碱收缩引起。这会导致痴呆症、记忆力丧失、学习能力和定向能力下降。在这项研究工作中，我们旨在探讨甲基莲心碱对AICI_3诱导的大鼠AD的神经保护作用。我们的研究结果表明，海马中活性氧（ROS）和一氧化氮的增加导致大鼠AD的发生。甲基莲心碱的口服治疗包括：；它可能抑制活性氧的形成，并通过防止神经退化而起到清除分子的作用。它还改善了AD大鼠完成迷宫活动的记忆和学习能力，并显著增加了经甲基莲心碱治疗的AD大鼠的抗氧化物超氧化物歧化酶、过氧化氢酶和还原型谷胱甘肽。积极降低神经退行性变大鼠模型中乙酰胆碱酯酶和Na~+K~+ATP酶的活性。在甲基莲心碱治疗的大鼠中，肿瘤坏死因子a（TNF-α）、白细胞介素6（IL-6）和白细胞介素1β（IL-1β）等神经炎症细胞因子的基因表达模式降低。奈非林治疗AD大鼠的神经炎症蛋白如诱导型一氧化氮（iNOS）、环氧合酶-2（COX-2）和核因子-κβ（Nf-κβ）减少，Nf-κβ抑制剂IKBα增加。最后，组织学研究证明，甲基莲心碱治疗可能预防AD模型海马组织的神经退行性变。因此，所有这些发现都表明，甲基莲心碱可能是神经和认知功能障碍中潜在的神经预防和神经退行性治疗化合物。

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