Action of low doses of Aspirin in Inflammation and Oxidative Stress induced by aβ<sub>1-42</sub> on Astrocytes in primary culture
Adrián Jorda, Martı́n Aldasoro, Constanza Aldasoro, Sol Guerra‐Ojeda, Antonio Iradi, José M. Vila, Juan Campos-Campos, Soraya L. Vallés
Abstract
Aspirin has been used as anti-inflammatory and anti-aggregate for decades but the precise mechanism(s) of action after the presence of the toxic peptide A1-42 in cultured astrocytes remains poorly resolved. Here we use low-doses of aspirin (10 -7 M) in astrocytes in primary culture in presence or absence of A1-42 toxic peptide. We noted an increase of cell viability and proliferation with or without A1-42 peptide presence in aspirin treated cells. In addition, a decrease in apoptosis, determined by Caspase 3 activity and the expression of Cyt c and Smac/Diablo, were detected. Also, aspirin diminished necrosis process (LDH levels), pro-inflammatory mediators (IL- and TNF-) and NF-B protein expression, increasing anti-inflammatory PPAR- protein expression, preventing A1-42 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 A1-42. Taken together, our results show that aspirin, at low doses increases cell viability by decreasing inflammation and oxidative stress, preventing the deleterious effects of the A1-42 peptide on astrocytes in primary culture. The use of low doses of aspirin may be more suitable for Alzheimer's disease.