Abstract：Objective：To observe the effect of Fuzheng Quji tang on the lung adenocarcinoma cells HCC827 resistance to icotinib， and discuss its possible mechanism. Methods： Human non- small cell lung adenocarcinoma cells HCC827 and medicine- resistant strain of icotinib HCC827 IR were cultured in vitro. The resistance of HCC827 and HCC827 IR to icotinib was detected. HCC827 IR cells treated with icotinib were divided into the HCC827 IR and low-dose Fuzheng Quji tang group (the HCC827 IR and low-dose group)，the HCC827 IR and middle-dose Fuzheng Quji tang group(the HCC827 IR and middledose group)，and the HCC827 IR and high- dose Fuzheng Quji tang group(the HCC827 IR and high- dose group). In each group，the inhibition rates of cell proliferation were detected through cell counting kit-8(CCK-8)，and cell apoptosis rate was detected through flow cytometry. The related-protein expression of hepatocyte growth factor(HGF)/c-Met signaling pathway was detected by western blot(WB). Results：Compared with those in the HCC827 group，in the HCC827 IR group，HGF， p-c-Met/c-Met，phosphatidylinositol-3 kinase(PI3k)/PI3K，and phosphorylated protein kinase B(p-Akt)/Akt were significantly increased(P＜0.05)，and the inhibition rates of cell proliferation，and apoptosis rats were significantly decreased(P＜0.05). Compared with those in the HCC827 IR group，in the HCC827 IR and low-dose，HCC827 IR and middle-dose，and HCC827 IR and high-dose groups，the inhibition rates of cell proliferation，and apoptosis rates were increased(P＜0.05)；HGF，p-cMet/c- Met， p- PI3K/PI3K， and p- Akt/Akt was decreased(P＜0.05)， and in a dose- dependent manner. Conclusion： Fuzheng Quji tang probably inhibits the resistance of non-small cell lung adenocarcinoma medicine-resistant strain to icotinib by inhibiting activation of HGF/c-Met pathway.