Fig. 4

Brassicasterol inhibits HBV + HCC cell growth through AKT signaling pathway. A–B HepG2.215 cells were first either untreated, mock-treated or treated brassicasterol for 48 h and then the expression cleaved caspase 3, AKT, p-AKT, ERK1/2 and p-ERK1/2 was measured by western blot. A One representative data of three is shown. B Densitometry analysis of western blot data was performed with Image J. Data shown are mean ± SD of three independent experiments. C PLC5 and D HepG2.215 cells were either mock-treated or treated with brassicasterol in the presence or absence of AKT agonist for 48 h, and then cell viability was assessed by MTT assay. Data shown are mean ± SD of three independent experiments. ^*, p < 0.05; ^**, p < 0.01; ^***, p < 0.001