Abstract: Objective To explore the inhibitory effect of polydatin on the proliferation and invasion in lung cancer A549 cells and its mechanism. Methods The lung cancer A549 cells were treated with different concentrations of polydatin (0, 10, 20, 50, 100 and 200 mg / L) for 24, 48 and 72 hours. The proliferation of A549 cells was measured by tetrazolium nitrogen salt (MTS) assay to determine the concentration of subsequent experiments (10 mg/L and 20 mg/L for 48h). With different concentrations of polydatin (0, 10 and 20 mg/L) for 48 hours, the invasion of A549 cells was measured by Transwell assay. The expression levels of matrix metalloprotinase (MMP)-2/9, integrin β4, Toll-like receptor (TLR3), cluster of differentiation (CD44) and phosphorylation of serine/threonine kinase (p-AKT) were measured by Western blotting and real-time PCR assay. The content of transforming growth factor (TGF) - β and tumor necrosis factor (TNF) - α in culture medium were measured by ELISA assay. The activity of nuclear factor (NF) - κB was measured by report gene assay.Results In the concentration ranges of 0, 10, 20, 50, 100 and 200 mg/L polydatin for 24, 48 and 72 h, the cell proliferation was decreased, and 10 mg/L and 20 mg/L of polydatin treatment for 48 h were used for following experiments. After treatment with polydatin for 48 h, the invasion was decreased, the contents of TGF-β and TNF-α were decreased, and the expression levels of MMP-2 / 9, integrin β4, TLR3, CD44, p-AKT and the activity of NF - κB were also decreased (P＜0.05).Conclusion Polydatin can inhibit the proliferation and invasion of lung cancer A549 cells by regulating the expression of tumor reated gene and the activity of AKT/NF-κB signal pathway.

Key words: lung neoplasms, cell proliferation, neoplasm invasiveness, polydatin, A459 cell