Fig 2. Cilostazol increases PGI₂ production via the arachidonic acid cascade.

(A) Effect of the COX inhibitor, indomethacin, on cilostazol-induced PGI₂ production (n = 5; † p < 0.05 vs. vehicle, t-test; * p < 0.05, ** p < 0.01 vs. 30 μM cilostazol, lower-tailed Williams’ test). (B) Top, Representative immunoblot showing pMAPK and MAPK expression in HAECs. Bottom, Effect of the MEK inhibitor, PD98059, on PGI₂ production in HAECs (n = 4, †† p < 0.01 vs. vehicle, t-test; ** p < 0.01 vs. 30 μM cilostazol t-test). (C) Top, Representative immunoblot showing p-cPLA₂ (Ser-505) and total cPLA₂ expression in HAEC. Bottom, Effect of AACOCF3 on cilostazol-induced PGI₂ production (n = 5; † p < 0.05, vs. vehicle, t-test; ** p < 0.01 vs. 30 μM cilostazol, lower-tailed Williams’ test). (D) Effect of cilostazol on intracellular calcium levels in HAECs. Fluo-4-loaded HAECs were pretreated with 100 μM BAPTA-AM for 15 min, and then cells were treated with cilostazol (30 μM, 50 s) followed by stimulation with 1 μM ionomycin (n = 4).