Figure 4

Effect of galangin on TPA-induced the PKCα , PKCδ activation and ERK phosphorylation in HepG2 cells. (A) Cells were treated with TPA (70 nM) for various times, the protein levels of PKCα, PKCβ, PKCδ, PKCθ, PKCλ, and PKCμ in the membrane fraction were analyzed. (B) Cells were treated with various concentrations (0, 1, 2.5, and 5 μM) of galangin in the presence or absence of TPA (70 nM) for 6 h, the protein levels of PKCα, PKCβ, PKCδ, PKCθ, PKCλ, and PKCμ in the membrane fraction was analysed. (C) Cells were treated with TPA (70 nM) for 2 h in various concentrations (0, 1, 2.5, and 5 μM) of galangin for 6 h. The JNK phosphorylation, JNK, ERK phosphorylation, ERK, p38 phosphorylation, p38, Akt phosphorylation, and Akt were analysed by Western blotting. β-Actin was used as a loading control. The relative density of phosphorylated forms of JNK, ERK, and p38 were normalized to total values of JNK, ERK, and p38, which were determined by densitometric analysis.