To study the inhibition effects of Qingfeixiaoji granules (QFXJ) on Lewis lung cancer mice and the apoptosis of tumor cells,45 male C57BL/6J mice were selected to build the Lewis lung cancer mouse model.They were randomly divided into model group (Mod),cisplatin group (DDP),low dose QFXJ group (QFXJ-L),middle dose QFXJ group (QFXJ-M),and high dose QFXJ group (QFXJ-H),with nine mice in each group.Other nine C57BL/6J mice were selected as the control group (Con).DDP was intraperitoneally injected with 0.2 mL cisplatin (according to 2 mg/kg) once every two days,and QFXJ-L,QFXJ-M,and QFXJ-H groups were intragastrically injected with 0.4 mL QFXJ in sequence (according to 12,24,and 48 g/kg,respectively) once a day.After 14 days of continuous administration,the tumor inhibition rate was calculated by stripping the tumor tissues and collecting blood.Hematoxylin-eosin (HE) staining was used to observe the pathological status of tumor tissues.Enzyme-linked immunosorbent assay (ELISA) was applied to determine the contents of tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),and interleukin-1β (IL-1β).The expression levels of phosphatidylinositol 3 kinase (PI3K),phosphorylated protein kinase B (p-AKT),B cell lymphocyte tumor 2 (Bcl-2),Bcl-2 associated X protein (Bax),and cysteinyl aspartate specific proteinase-3 (Caspase-3) in tumor tissues were determined with Western blot (WB).Cell apoptosis in tumor tissues was observed with TdT-mediated dUTP nick-end labeling (TUNEL) technology.The results showed that the tumor weight of QFXJ-M,QFXJ-H,and DDP was significantly decreased compared with Mod (P < 0.05).The tumor histopathological results suggested that the density of tumor cells in QFXJ-L,QFXJ-M,and QFXJ-H decreased to varying degrees,and the density of necrotic cells increased.The expressions of TNF-α,IL-6,and IL-1β in the serum of QFXJ-M,QFXJ-H,and DDP were significantly decreased (P < 0.05).The protein expression levels of PI3K,p-AKT,and Bcl-2 were decreased in tumor tissues of QFXJ-H and DDP,while the expression levels of Bax and Caspase-3 were significantly increased (P < 0.05).TUNEL fluorescence results showed that the number of positive cells in each drug administration group was higher than that in the model group.In conclusion,QFXJ may regulate the relevant targets of PI3K/AKT signaling pathway,up-regulat the expressions of pro-apoptotic proteins Bax and Caspase-3,and down-regulat the expressions of anti-apoptotic protein Bcl-2,and thus promote the apoptosis of lung cancer cells and inhibit the growth of lung cancer tissues.