Fig. 7.
Fig. 7. Effect of MEK inhibitor PD98 059 and p38 inhibitor SB202 190 on eotaxin-induced ECP release. / Eosinophils were preincubated with buffer, PD98 059 (1-50 μM), or SB202 190 (0.5-10 μM) for 1 hour and stimulated with eotaxin (10−7 mol/L) for 4 hours. ECP release was measured by radioimmunoassay. The number of eosinophil donors for PD98 059 and SB202 190 experiments were 4 and 3, respectively. The results are shown as the mean ± SD of ECP release from 106 cells. The values were corrected for the ECP release in buffer, which were 7.6 ± 3 and 6.9 ± 2.3 ng per 106 cells for PD98 059 and SB202 190 experiments, respectively. The inhibition of ECP release by 5, 10, and 50 μM of PD98 059 and by all tested concentrations of SB202 190 was statistically significant (*P < .05).

Effect of MEK inhibitor PD98 059 and p38 inhibitor SB202 190 on eotaxin-induced ECP release.

Eosinophils were preincubated with buffer, PD98 059 (1-50 μM), or SB202 190 (0.5-10 μM) for 1 hour and stimulated with eotaxin (10−7 mol/L) for 4 hours. ECP release was measured by radioimmunoassay. The number of eosinophil donors for PD98 059 and SB202 190 experiments were 4 and 3, respectively. The results are shown as the mean ± SD of ECP release from 106 cells. The values were corrected for the ECP release in buffer, which were 7.6 ± 3 and 6.9 ± 2.3 ng per 106 cells for PD98 059 and SB202 190 experiments, respectively. The inhibition of ECP release by 5, 10, and 50 μM of PD98 059 and by all tested concentrations of SB202 190 was statistically significant (*P < .05).

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