Objective: To explore the mechanism of Jinfukang oral liquid (JFK) in inducing the apoptosis of non-small cell lung cancer cell line A549. Method: The non-small cell lung cancer cell lines A549 in logarithmic phase of growth were randomly divided into the control group and drug treatment groups. The 3-(4

5-dimethylthiazol-2-yl)-2

5-diphenyltetrazolium bromide (MTT) assay was used to investigate the effects of different concentrations of JFK (0.3

1.5

3

7.5

15

30 g · L-1) on the proliferation of A549 cells in vitro. The plate colony formation assay and flow cytometry were used to observe the effects of JFK on the colony formation and apoptosis of A549 cells

respectively. Protein expressions of cleaved PARP

active Caspase-3

β-catenin

cyclinD1

and the mitogen-activated protein kinase(MAPK)/proteinkinse B(Akt) signaling pathways were investigated by Western blot. Cells were divided into control group and drug groups treated at the concentrations of 15

30 g · L-1

and each group was intervened for 24 h or 30 min. Result: JFK inhibited the proliferation of A549 cells in a dose-dependent manner within the range from 1.5-30 g · L-1(P<0.01). JFK inhibited colony formation at 15-30 g · L-1(P<0.01). JFK increased the ratio of Annexin V and PI double positive cells at the concentrations of 15-30 g · L-1

suggesting that JFK induced apoptosis in A549 cells (P<0.05). The protein expressions of cleaved PARP and activated Caspase-3 were increased

while the expressions of β-catenin and cyclinD1 were suppressed in a dose-dependent manner (P<0.05

P<0.01) after treatment with JFK. And the phosphorylation levels of JNK and p38 were up-regulated

while that of T308 and S473 sites of Akt were down-regulated (P<0.05). Conclusion: Jinfukang decoction inhibited the proliferation and colony formation of non-small cell lung cancer cells A549.JFK induced apoptosis with the increase of the protein expressions of cleaved PARP and activated Caspase-3

and the decrease of the protein expressions of β-catenin and cyclinD1

partly through JNK/p38/MAPK and Akt signaling pathways.