Objective To study the effect of trichosanthin（ TCS） on cell apoptosis of lung cancer cell line A549 and explore its possible mechanism of action.Methods The human lung adenocarcinoma cell line A549 in exponential growth period was selected.The cell concentration was adjusted to 2 × 104/ml and inoculated in 96-well plate.After pre-culture for 24 hours

TCS injection was added.Finally

the concentration of TCS in each group was adjusted to 0.04 mg /ml

0.08 mg /ml

0.12 mg /ml and 0.16 mg /ml respectively.Each dosage was made in quadruplicate and the normal cell group was set as control.The cells were cultured for 24 hours.The apoptosis cells were counted under light microscope and the apoptotic index was calculated at 24 h

48 h and 72 h.The JNK specific inhibitor SP600125 was chosen and four groups such as blank control group

SP 600125 group（20nmol /L

100 μl）

TCS group（0.12mg/ml

100μl） and TCS and SP600125 group（ 100μl） were set.The expressions of JNK and Bcl-2 in each group were detected with Western blot method.Results Comparing with the control group

the apoptotic index was significantly increased in 0.08 mg /ml

0.12 mg /ml and 0.16 mg /ml groups at each time point except 0.08 mg /ml group at 24 h（ P < 0.05 or P < 0.01）.Comparing with at 24 h

the apoptotic index was significantly increased at 48h in 0.04 mg /ml group（ P < 0.05）.Comparing with 0.04 mg /ml group at 24 h

the apoptotic index was significantly increased in 0.08 mg /ml group

0.12 mg /ml group and 0.16 mg/ml group at 32 h and 48 h（ P<0.05）.Comparing with SP600125 group

the JNK expression of A549 cell was significantly increased but the Bcl-2 expression was significantly decreased in TCS group and TCS and SP600125 group（P 0.05）.Comparing with TCS group

the JNK expression of A 549 cell was significantly decreased but Bcl-2 expression was significantly increased in TCS and SP600125 group（ P < 0.05）.Conclusion TCS may induce the decrease of Bcl-2 expression of lung adenocarcinoma cell line A549 by activating JNK signaling pathway to cause cell apoptosis.