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Figure 2. Effect of caffeic acid phenethyl ester on IK in normal human oral keratinocytes. (A) Original current tracings obtained when the cell was held at –40 mV and the ramp pulses from –80 to +100 mV with a duration of 1 sec were applied. "a" is the control, "b" was recorded in the presence of caffeic acid phenethyl ester (10 µM), and "c" was obtained after the application of caffeic acid phenethyl ester plus paxilline (1 µM). (B) Concentration-dependent stimulation of caffeic acid phenethyl ester on IK in normal human oral keratinocytes. Each cell was depolarized from –40 to +50 mV. Current amplitude in the presence of 300 µM caffeic acid phenethyl ester was considered to be 100%. The smooth line is the fit of the data with a Hill function as described in MATERIALS & METHODS. The values for EC50, maximally stimulated percentage of IK, and the Hill coefficient were 12.8 ± 1.2 µM, 99 ± 1%, and 1.2 ± 0.1 (n = 5). (C) Bar graph showing the effects of caffeic acid phenethyl ester, cinnamyl-3,4-dihydroxy-{alpha}-cyanocinnamate, nordihydroguaiaretic acid, caffeic acid phenethyl ester plus paxilline, and caffeic acid phenethyl ester plus anandamide on the amplitude of IK. Each cell was depolarized from –40 to +50 mV. Current amplitudes were measured at the end of depolarizing pulses. The amplitude in the control was considered to be 1.0, and the relative amplitudes during exposure to each agent were compared. Mean ± SEM (n = 5–7). CAPE, caffeic acid phenethyl ester (10 µM); CDC, cinnamyl-3,4-dihydroxy-{alpha}-cyanocinnamate (10 µM); NDGA, nordihydroguaiaretic acid (10 µM); Pax, paxilline (1 µM); and Anan, anandamide (10 µM). *Significantly different from the control group. **Significantly different from the group with caffeic acid phenethyl ester alone.