| Objective To study the effects of hedyotis diffusa extract (HDE) on the proliferation and apoptosis of hepatoma QGYcells, and to explore the possible mechanism of its anti-tumor effect.Methods The QGY cells were cultured in vitro and divided into control group: cultured in RPMI-1640 culture medium; positive control group: all trans retinoic acid (AT-RA) (5 μmol/L); low, mediumand high dose groups of Hedyotis diffusa extract (HDE): 20, 40 and 80 g/L HDE respectively. MTT method was used to detect cell pro-liferation, Hoechst33258 fluorescence staining and flow Annexin V-FITC/PI double staining were used to detect the apoptosis rate; in addition, the levels of proliferating cell nuclear antigen (PCNA), B-lymphoma gene-2 (Bcl-2), Bcl-2 related X protein gene (Bax), cas- pase-3 and JNK/p38MARK pathway related proteins were detected by Western blotting.Results Compared with those in the controlgroup[(16.56±3.15)%,(19.27±3.33)%] at the same time point, the inhibition rate of QGY cell proliferation in 20, 40, 80 g/L HDE groups[24 h(33.37±11.36)%,(47.57±13.62)%,(59.37±16.95)%,48 h(36.56±10.03)%,(50.59±13.87)%,(63.61±16.99)%] and positive controlgroup[(60.43±17.09)%,(64.63±17.15)%] at 24, 48 h increased significantly (P<0.05). Compared with those in the control group, the apoptosis rate, Bax and caspase-3 protein of QGY cells after treatment with HDE with concentration of 20, 40 and 80 g/L increased sig-nificantly (P < 0.05), the expressions of PCNA, Bcl-2 protein, p-JNK/JNK, p-p38/p38 decreased (P<0.05), and all of them were concen- tration dependent, while there was no significant difference in apoptosis rate, Bax, Caspase-3, PCNA, Bcl-2 protein, p-JNK/JNK, p-p38/ p38 expressions between the 80 g/L HDE group and the positive control group (P>0.05).Conclusion HDE can inhibit the prolifera- tion of QGY cells of liver cancer and promote the apoptosis of QGY cells, which may play an anti-tumor role by inhibiting the activation of JNK/p38MARK pathway. |
