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. 2016 Jun 8;11(6):e0157186. doi: 10.1371/journal.pone.0157186

Fig 4. Effect of simvastatin treatment on CCR3 and downstream activation of ERK1/2 and p38 in BA-E cells.

Fig 4

(A) BA-E cells were pretreated with 0–25 μM simvastatin for 3 h and stimulated by 10 ng/ml IL-5 for 24 h. Presentation of CCR3 measured by real-time PCR was inhibited by simvastatin treatment in dose-dependant manner if BA-E cells treated with simvastatin no more than 25 μM. (B) CCR3 expression (green) on the surface of BA-E cells was revealed by immunocytochemical stain in different treatments. (C) BA-E cells were pretreated with/without 25 μM simvastatin for 3 h, followed by 10 ng/ml IL-5 for 24 h and 100 ng/ml eotaxin was added for 0, 30, 60 and 90 min. The activations of ERK1/2 and p38 were analyzed by Western blot with the use of antibodies against phosphorylated ERK1/2 and phosphorylated p38 MAPK. Data were expressed as the combined mean ± SEM of n = 5 independent experiments. #P < 0.01, compared with BA-E cells without IL-5 treatment; *P < 0.05, compared with IL-5 primed BA-E cells without simvastatin treatment, Mann–Whitney U test.