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. 2017 Aug 16;12(8):e0182981. doi: 10.1371/journal.pone.0182981

Fig 5. 18β-GA-d increased the phosphorylation of Akt, ERK1/2, and p38 in human dermal fibroblasts.

Fig 5

(A) Human dermal fibroblasts were treated with 0.1% THF or 18β-GA-d (30 μM) for different times. The level of phosphorylation of Akt, ERK1/2, and p38 at different times was analyzed by western blot assay. The quantification data for the ratios of phosphorylated protein/total non-phosphorylated protein in THF- and 18β-GA-d- treated groups to those in the untreated groups are shown in the lower panels. *p < 0.05 compared with THF treatment at the same time point (mean ± S.E.M. n = 3). (B) Human dermal fibroblasts were pretreated with UO126 (ERK inhibitor) (20 μM), MK2206 (Akt inhibitor) (5 μM), or SB203580 (p38 inhibitor) (10 μM) and then treated with 0.1% THF or 18β-GA-d (30μM) for 24 h. The protein expression of AQP-3 was evaluated by western blot assay. The quantification data for ratios of AQP-3/α-tubulin in different groups, relative to AQP-3/α-tubulin in the THF-treated group, are shown in the right panel. *p < 0.05 (mean ± S.E.M. n = 3).