Constanza Aldasoro
University of Valencia, Spain
Title: Action of low doses of aspirin in inflammation and oxidative stress induced by aβ1-42 on astrocytes in primary culture
Biography:
Abstract:
Alzheimer’s disease (AD) causes decline in memory and is the most common neurodegenerative disease implicated in the aging process (Lane et al. 2018). The prominent features of AD include amyloid plaques, intraneuronal tangles, cell death, inflammatory changes and oxidative stress (Perry et al. 2002; Selkoe et al. 2016). In this study, we were interested in exploring the action of aspirin in both inflammatory and ROS (reactive oxygen species) events associated with Alzheimer’s disease (AD) by using the amyloid β1-42 in astrocytes in primary culture. Aspirin diminished pro-inflammatory mediators (IL-β and TNF-α) and NF-á´‹B protein expression, increasing anti-inflammatory PPAR-γ protein expression, preventing Aβ1-42 toxic effects. Aspirin inhibited COX-2 and iNOS without changes in COX-1 expression, increasing anti-oxidant protein (Cu/Zn-SOD and Mn-SOD) expression in presence or absence of Aβ1-42. The key finding of our study, is that at low doses of aspirin a recovery of oxidative stress and inflammation, induced previously by Aβ1-42 toxic peptide on astrocytes in primary culture, was detected. This indicates that administration of low dose of aspirin to AD patients, could be more useful than high doses.