Figure 8. NSAIDs inhibit cytochrome c release and cell death induced by Aβ_1–42 oligomers.

A,B. Cerebellar granule cells were treated with Aβ_1–42 (500 nM) for 72 h with or without 1 µM R-flurbiprofen or 100 µM salicylate and fixed for analysis of cytochrome c location using confocal microscopy. A. Control cells showed a punctate distribution of cytochrome c. Scale bar represents 10 µm. Aβ_1–42 oligomers-treated cells show a more diffuse pattern of cytochrome c whereas cells treated with Aβ_1–42 oligomers plus R-flurbiprofen show a punctate pattern similar to control cells. B. Bars show the relative abundance (%) of cells showing diffuse immunostaining in control cells, cells treated with Aβ_1–42 oligomers and cells treated with Aβ_1–42 oligomers plus 1 µM R-flurbiprofen or 100 µM salicylate (B). *p<0 05 vs control; #p<0 05 vs Aβ; data from at least 3 independent experiments. Salicylate 100 µM inhibits cell death induced by Aβ_25–35 (20 µM) in cerebellar granule cells (C) and GT1 cells (D). Salicylate 100 µM also inhibits cell death induced by Aβ_1–42 oligomers (500 nM) in cerebellar granule cells (E). (*p<0 05 vs control; #p<0 05 vs Aβ. n = 3). F. Ibuprofen (Ibu), Indomethacin (Indo), and sulindac sulfide (Sul), all tested at 1 µM, inhibit cell death induced by Aβ_1–42 oligomers (500 nM) in cerebellar granule cells. G. R-Flurbiprofen 1 µM also inhibits cell death induced by Aβ_1–42 oligomers (500 nM). *p<0 05 vs. control; ^#p<0 05 vs Aβ. All data are representative of 3 experiments.