Abstract: Objective　To investigate the effects and mechanisms of sennoside B on the growth, invasion of A549 cells and tumorigenesis of nude mice.　Methods　A549 non-small cell lung cancer cells were treated with sennoside B at doses of 0, 5, 10 and 20 μM respectively. The cells were divided into four groups randomly according to the dose and then the follow-up experiment was proceeded. Brdu staining was used to detect the cell proliferation of each group, and Hoechst staining was used to detect apoptosis. Cell migration was detected by scratch test. Cell invasion was detected by Transwell assay. Protein expression levels of Ki67, PCNA, cl-caspase-3, cl-caspase-9, VEGF, N-cadherin and E-cadherin, as well as phosphorylation of STAT3 and ERK1/2 were detected by western blotting. Tumor-bearing mice model was established and the weight of tumor was tested. The expression of Ki67 and VEGF were detected by immunohistochemistry.　Results　Compared with the Control group, the result showed that the Brdu positive cells number, the invasion cells number in each sennoside B dosage group were significantly reduced（P<0.05）, the apoptosis rate increased significantly（P<0.05）, the rate of cells scratches healing（P<0.05）, the protein levels of ki67, PCNA and VEGF, N-cadherin decreased obviously（P<0.05）, the protein levels of cl-caspase-3, cl-caspase-9, E-cadherin increased significantly（P<0.05）, phosphorylation levels of STAT3 and ERK1/2 were significantly reduced （P<0.05）, and the weight of tumor and the expression levels of Ki67 and VEGF were decreased in tumor-bearing mice model（P<0.05）.　Conclusions　Sennoside B inhibits the phosphorylation of STAT3 and ERK1/2 and the growth of A549 cells.

Key words:  Non-small cell lung cancer, 　Sennoside B;　STAT3, 　ERK1/2