Aluminum is a potent neurotoxin used in animal models of neurodegenerative diseases like Alzheimer's disease (AD), in which oxidative stress mediates tissue pathogenesis in vivo. N-acetyl cysteine (NAC) is a glutathione precursor with reported antioxidant and neuroprotective potentials. Recent therapy for combating AD is known to provide only symptomatic relief thus necessitating the discovery of new drugs and their mechanism of action. This study was aimed to demonstrate the in vivo neuroprotective effect of NAC against aluminum (Al3+)-induced neuro-degeneration in rats (a model for AD). Twenty- five (25) adult male Wistar rats used for this study were divided into 5 groups: Group A = Control, B = Aluminum chloride (200 mg/kg), C = 1000 mg/kg of NAC + Aluminum chloride (200 mg/kg), D = 1000 mg/kg of NAC, E = Aluminum chloride (200 mg/kg) was orally administered daily for 3 weeks and discontinued for one week. Frontal Cortex harvested for histological analysis using Haematoxylin and Eosin stain, Cresyl Fast Violet stain for Nissl granules and Glial fibrillary acidic protein immunohistochemistry specific for astrocytes. Aluminum significantly induced oxidative stress, coupled with marked neurons necrosis, chromatolysis and gliosis in the frontal cortex, upon NAC administration, there was neuro anti-inflammatory response as seen in the significant reduction in astrocytes expression, neuronal cell death and Nissl body aggregation which attenuates neuropathological deficits induced by Al3+. It was shown that aluminum is a neurotoxin mediating AD-like oxidative stress, NAC has a therapeutic potential associated with its potent in vivo interaction with astrocytes in response to Al3+ neuro-inflammation seen in positive expression of Nissl granules and glial cells in addition to possibility of endogenous glutathione neuroprotection after withdrawal of stress mediator in neurodegeneration. Graphical abstract.

中文翻译：

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在铝诱导的神经变性大鼠模型中给予 N-乙酰半胱氨酸后额叶皮质锥体外系细胞层的组织形态学评估。


铝是一种强效神经毒素，用于阿尔茨海默氏病（AD）等神经退行性疾病的动物模型，其中氧化应激介导体内组织发病机制。 N-乙酰半胱氨酸 (NAC) 是一种谷胱甘肽前体，据报道具有抗氧化和神经保护潜力。众所周知，最近对抗 AD 的疗法只能缓解症状，因此需要发现新药及其作用机制。本研究旨在证明 NAC 对铝 (Al3+) 诱导的大鼠神经变性（AD 模型）的体内神经保护作用。用于本研究的二十五 (25) 只成年雄性 Wistar 大鼠被分为 5 组：A 组 = 对照组，B = 氯化铝 (200 mg/kg)，C = 1000 mg/kg NAC + 氯化铝 (200 mg/kg) /kg)，D = 1000 mg/kg NAC，E = 氯化铝 (200 mg/kg)，每天口服给药 3 周，并停药 1 周。使用苏木精和伊红染色剂、尼氏颗粒的甲酚固紫染色剂和星形胶质细胞特异性的神经胶质原纤维酸性蛋白免疫组织化学收获额叶皮层进行组织学分析。铝显着诱导氧化应激，加上额叶皮质中明显的神经元坏死、色素溶解和神经胶质增生，在给予 NAC 后，出现神经抗炎反应，表现为星形胶质细胞表达显着减少、神经元细胞死亡和尼氏体聚集减弱。 Al3+ 诱导的神经病理学缺陷。 结果表明，铝是一种介导 AD 样氧化应激的神经毒素，NAC 具有治疗潜力，与其在尼氏颗粒和神经胶质细胞阳性表达中观察到的 Al3+ 神经炎症反应中与星形胶质细胞的有效体内相互作用有关。神经变性中应激介质撤除后内源性谷胱甘肽的神经保护作用。图形摘要。