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. 2014 Aug 15;9(8):e104743. doi: 10.1371/journal.pone.0104743

Figure 5. Increased SIRT1 expression and deacetylase activity by cilostazol.

Figure 5

(A) Time (3–24 hr)-dependent decrease in SIRT1 protein expression after exposure to HMGB1 (100 ng/ml), and (B) recovery of reduced SIRT1 expression by cilostazol (1–30 µM) and by resveratrol (RES, 20 µM). (C) HMGB1-induced increase in H4 acetyl-k16 (H4 Ac-K16) immunoreactivity was decreased by cilostazol (10 and 30 µM) and resveratrol (RES, 20 µM). Cilostazol-induced decrease in H4 Ac-K16 was prevented by sirtinol (20 µM). (D) Analyses of SIRT1 knockout RA SFs compared with negative control cells. Cilostazol (10 µM) failed to induce expression of SIRT1 in RA SF cells transfected with SIRT1 siRNA oligonucleotide (100 nM) as contrasted to negative control. (E and F) Loss of the effect of cilostazol on the elevated expressions of p65 and acetyl (AC)-p65 induced by HMGB1 (100 ng/ml) in SIRT1 gene silenced fibroblasts, which contrasted to the effects of cilostazol in the negative control cells. Results are the means ±SEM of 4 experiments. **P<0.01, ***P<0.001 vs. no treatment or vehicle (Veh); ## P<0.01, ### P<0.001 vs. HMGB1; †† P<0.01 vs. 10 µM cilostazol.