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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Acetaminophen protects hippocampal neurons and PC12 cultures from amyloid beta-peptides induced oxidative stress and reduces NF-kappaB activation.
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Acetaminophen protects hippocampal neurons and PC12 cultures from amyloid beta-peptides induced oxidative stress and reduces NF-kappaB activation.

机译：对乙酰氨基酚可保护海马神经元和PC12培养物免受淀粉样β肽诱导的氧化应激并降低NF-κB的活化。

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摘要

The present findings show that an atypical non-steroidal anti-inflammatory drug, such as acetaminophen, retains the ability to recover amyloid beta-peptides driven neuronal apoptosis through the impairment of oxidative stress. Moreover, this compound reduces the increased NF-kappaB binding activity, which occurs in these degenerative conditions.Therapeutic interventions aimed at reducing the inflammatory response in Alzheimer's disease (AD) recently suggested the application of non-steroidal anti-inflammatory drugs. Although the anti-inflammatory properties of acetaminophen are controversial, it emerged that in an amyloid-driven astrocytoma cell degeneration model acetaminophen proved to be effective.On these bases, we analyzed the role of acetaminophen against the toxicity exerted by different Abeta-peptides on rat primary hippocampal neurons and on a rat pheochromocytoma cell line. We found a consistent protection from amyloid beta-fragments 1-40 and 1-42-induced impairment of mitochondrial redox activity on both cell cultures, associated with a marked reduction of apoptotic nuclear fragmentation. An antioxidant component of the protective activity emerged from the analysis of the reduction of phospholipid peroxidation, and also from a significant reduction of cytoplasmic accumulation of peroxides in the pheochromocytoma cell line. Moreover, activation of NF-kappaB by amyloid-derived peptides was greatly impaired by acetaminophen pre-treatment in hippocampal cells.This evidence points out antioxidant and anti-transcriptional properties of acetaminophen besides the known capability to interfere with inflammation within the central nervous system, and suggests that it can be exploited as a possible therapeutic approach against AD.
机译：目前的发现表明，非典型的非甾体类抗炎药，如对乙酰氨基酚，保留了通过氧化应激损伤恢复淀粉样β肽驱动的神经元凋亡的能力。此外，该化合物降低了在这些退化条件下发生的增加的NF-κB结合活性。旨在减少阿尔茨海默氏病（AD）中炎症反应的治疗性干预最近建议使用非甾体抗炎药。尽管对乙酰氨基酚的抗炎特性存在争议，但发现在淀粉样蛋白驱动的星形细胞瘤细胞变性模型中，对乙酰氨基酚被证明是有效的。在这些基础上，我们分析了对乙酰氨基酚对不同Abeta肽对大鼠产生的毒性的作用。原代海马神经元和大鼠嗜铬细胞瘤细胞系上。我们发现在两种细胞培养物中均不受淀粉样蛋白β片段1-40和1-42诱导的线粒体氧化还原活性损伤的一致保护，并与凋亡核分裂的明显减少相关。具有保护活性的抗氧化剂成分来自磷脂过氧化减少的分析，也来自嗜铬细胞瘤细胞系中过氧化物的细胞质积累的显着减少。此外，对乙酰氨基酚预处理对海马细胞的淀粉样蛋白衍生肽激活NF-κB的作用大大减弱，这表明对乙酰氨基酚的抗氧化和抗转录特性除了已知的干扰中枢神经系统炎症的能力外，并建议将其开发为抗AD的可能治疗方法。

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