铝的使用和毒性一直是全球关注的问题,特别是来自环境和工作场所的纳米颗粒铝(Al-NP)产品的使用增加。由于人体中的常规生物修复过程,Al在环境中降解为纳米颗粒形式。Al-NPs毒性在神经变性的病理生理学中起着关键作用,神经变性的特征是与阿尔茨海默病相关的神经原纤维缠结和神经炎斑块的发展。这项研究评估了Al-NP诱导的神经变性和由氧化应激引起的行为改变,炎症,DNA损伤,β-淀粉样蛋白聚集,和小鼠的组织病理学变化。此外,评估了柚皮素(NAR)作为有效的神经保护性类黄酮对Al-NP诱导的神经变性的预防作用。Al-NP的合成和检测使用FTIR,XRD,TEM,和粒度分析仪。小鼠口服施用Al-NP(6mg/kgb.w.),随后NAR处理(10mg/kgb.w./天),持续66天。空间工作记忆是通过新颖的物体识别来确定的,T迷宫,Y-迷宫,和莫里斯水迷宫测试。我们测量了一氧化氮,蛋白质产品的高级氧化,蛋白质羰基化,脂质过氧化,超氧化物歧化酶,过氧化氢酶,谷胱甘肽过氧化物酶,谷胱甘肽还原酶,还原型谷胱甘肽,氧化谷胱甘肽,和乙酰胆碱酯酶,以及细胞因子分析,免疫组织化学,和DNA损伤。Al-NP显著降低了学习记忆能力,氧化应激增加,抗氧化酶活性降低,增加DNA损伤,改变了细胞因子的水平,并增加小鼠大脑皮质和海马区的β-淀粉样蛋白聚集。这些神经行为障碍,神经元氧化应激,补充NAR可显着减轻组织病理学改变。总之,Al-NP在暴露后可能具有强大的神经毒性,并且NAR可以作为治疗和管理神经元变性的潜在预防措施。
Alumunium usage and toxicity has been a global concern especially an increased use of nanoparticulated aluminum (Al-NPs) products from the environment and the workplace. Al degrades in to nanoparticulate form in the environment due to the routine process of bioremediation in human body. Al-NPs toxicity plays key role in the pathophysiology of neurodegeneration which is characterised by the development of neurofibrillary tangles and neuritic plaques which correlates to the Alzheimer\'s disease. This study evaluated the Al-NPs induced neurodegeneration and causative behavioral alterations due to oxidative stress, inflammation, DNA damage, β-amyloid aggregation, and histopathological changes in mice. Furthermore, the preventive effect of naringenin (NAR) as a potent neuroprotective flavonoid against Al-NPs induced neurodegeneration was assessed. Al-NPs were synthesized and examined using FTIR, XRD, TEM, and particle size analyzer. Mice were orally administered with Al-NPs (6 mg/kg b.w.) followed by NAR treatment (10 mg/kg b.w. per day) for 66 days. The spatial working memory was determined by novel object recognition, T-maze, Y-maze, and Morris Water Maze tests. We measured nitric oxide, advanced oxidation of protein products, protein carbonylation, lipid peroxidation, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, reduced glutathione, oxidised glutathione, and acetylcholine esterase, as well as cytokines analysis, immunohistochemistry, and DNA damage. Al-NPs significantly reduced the learning memory power, increased oxidative stress, reduced antioxidant enzymatic activity, increased DNA damage, altered the levels of cytokines, and increased β-amyloid aggregation in the cortex and hippocampus regions of the mice brain. These neurobehavioral impairments, neuronal oxidative stress, and histopathological alterations were significantly attenuated by NAR supplementation. In conclusion, Al-NPs may be potent neurotoxic upon exposure and that NAR could serve as a potential preventive measure in the treatment and management of neuronal degeneration.