Fig. 3.

Skin hydration effects of compound K (CK). (A) HaCaT cells were treated with CK for 24 h, and cells were harvested. Phosphorylation level of inhibitor of κBα and mitogen-activated protein kinases [c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38] were tested by immunoblotting. (B) HaCaT cells were pretreated with mitogen-activated protein kinases inhibitors (SB203580, SP600125, U0126) for 30 min and incubated in presence or absence of CK for 24 h. mRNA expression levels were determined by RT-PCR. (C) HEK293T cells were transfected with AP-1-Luc or cyclic adenosine monophosphate response element binding protein-Luc constructs and β-gal (as a control) for 24 h, and cells were treated with CK for an additional 24 h. Luciferase activity was measured using a luminometer. * p < 0.05 and ** p < 0.01 compared to the normal groups.