PMID: 11918971Mar 29, 2002Paper

Acetaminophen protects hippocampal neurons and PC12 cultures from amyloid beta-peptides induced oxidative stress and reduces NF-kappaB activation

Neurochemistry International
M BisagliaG Schettini

Abstract

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...Continue Reading

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Citations

Oct 20, 2009·The Journal of Membrane Biology·Mustafa NaziroğluRamazan Bal
Nov 26, 2003·Brain Research Bulletin·András PalotásJános Kálmán
Feb 20, 2003·Neurochemistry International·András PalotásBotond Penke
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Apr 12, 2003·Neurochemistry International·Zhi-Zhong GuanAgneta Nordberg
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