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. 2015 Aug 5;10(8):e0134486. doi: 10.1371/journal.pone.0134486

Fig 7. Effect of cilostazol on Aβ-induced cytotoxicity.

Fig 7

Decrease in cell viability in response to exogenous Aβ1–42 in N2a cells (A) and to endogenously overproduced Aβ in the N2aSwe cells (B), and the recovery by cilostazol in the absence and presence of 3-methyladenine (3-MA, 2.5 mM). Results are the means ± SDs of three experiments. ### P < 0.001 vs. PBS (A) and Tet- condition (B); ***P < 0.001 vs. DMSO; † P < 0.05, †† P < 0.01, ††† P < 0.001 vs. 10 or 30 μM cilostazol alone. PBS, phosphate-buffered saline. C. Hypothetical model: Neuroprotective effect of cilostazol against Aβ-induced neurotoxicity is ascribable to the increased induction of autophagy by increasing the cAMP/PKA coupled SIRT1 activation, thereby enhances Aβ and CTFβclearance and increases cell viability.