Fig. 6

ERK1/2-HNF4α axis contributed to EGCG inhibition of HBV core promoter activity. a The effect of ERK signaling on EGCG-mediated inhibition of HBV core promoter activity. The cells were transfected with a core promoter-dependent reporter plasmid (CpLUC). Twenty-four hours post transfection, the cells were treated with EGCG in the absence or presence of the ERK inhibitor PD98059 (20 μM), the p38 inhibitor 203580 (10 μM) or the JAK2/STAT3 inhibitor AG490 (50 μM) for 24 h, followed by the detection of luciferase activity in the cell lysates. b The effect of ectopic HNF4α expression on the EGCG-mediated inhibition of HBV promoter activity. The HNF4α expression plasmid (pHNF4α-HA) was transfected into HepG2.2.15 cells together with CpLUC. Twenty-four hours post transfection, the cells were further stimulated with EGCG for another 24 h, followed by the detection of luciferase activity. Below: The whole cell lysate was subjected to Western blotting using antibodies against HA and GAPDH. c The effect of HNF4α expression on EGCG-mediated inhibition of HBV gene expression and replication. HepG2.2.15 cells were transfected with control empty vector or an increasing dose of pHNF4α for 24 h and then treated with EGCG for another 24 h. HBeAg and HBV-DNA levels were determined by ELISA and qPCR, respectively. The values were expressed as the means ± SEM of three independent experiments; *P < 0.05; (unpaired, two-tailed Student’s t tests)