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