Action of low doses of Aspirin in Inflammation and Oxidative Stress induced by aβ1-42 on Astrocytes in primary culture

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 A beta(1)(-)(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 A beta(1)(-)(42) toxic peptide. We noted an increase of cell viability and proliferation with or without A beta(1)(-)(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-beta and TNF-alpha) and NF-kappa B protein expression, increasing anti-inflammatory PPAR-gamma protein expression, preventing A beta(1)(-)(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 A beta(1)(-)(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 A beta(1)(-)(42) peptide on astrocytes in primary culture. The use of low doses of aspirin may be more suitable for Alzheimer's disease.