Abstract: Objective The aim of this study was to explore the effects of britanin on cell proliferation and apoptosis and impact on mammalian target of rapamycin complex (mTORC1) signal pathway in HepG2 cells in vitro. Methods The Hep G2 cells were cultured with britanin at 0 μmol/L (control), 5 μmol/L, 10 μmol/L and 20 μmol/L for 48 hours. The cell proliferation was detected by MTT, the cell apoptosis was evaluated by flow cytometry, and the apoptosis-related protein expressions, such as Bax, Bcl2 and Caspase3 and mTORC1 signaling pathway were detected by Western bloting. Results The cell proliferation rates in 5 μmol/L, 10 μmol/L and 20 μmol/L britanin-intervened groups were (89.56±8.11)%, (66.40±6.61)% and (41.78±5.79)%, all significantly lower than [(100.00±10.01)%, P<0.05] in the control; the apoptosis rate were (14.75±1.34)%, (19.11±1.87) % and (27.45±1.99)%, significantly higher than [(7.01±0.89)%, P<0.05] in the control; the expressions of pro-apoptotic proteins, Bax and Caspase3, were (1.36±0.15) and (1.63±0.32), (3.57±0.33) and (3.92±0.47), and (7.33±0.52) and (6.94±0.53), all significantly higher than [(0.98±0.11) and (0.87±0.15), P<0.05] in the control, while the expression of anti-apoptotic protein, Bcl2, were (4.71±0.52), (2.36±0.36) and (0.89±0.14), significantly lower than [(8.05±0.65), P<0.05] in the control; the protein expressions of mTORC1 and 70S6K were (0.82±0.08) and (0.79±0.08), (0.63±0.06) and (0.58±0.05) and (0.51±0.05) and ( 0.43±0.04), all significantly lower than [(0.96±0.11) and (0.99±0.09), P<0.05] in the control. Conclusion Britanin could inhibit cell proliferation and induce cell apoptosis, which might exert a certain anti-tumor effects by down-regulation of mTORC1 signaling pathway.

Key words: HepG2 cells, Britanin, Proliferation, Apoptosis, mTORC1 signaling pathway