This study aims to investigate the effect of atractylenolide II (AT-II) on JAK2/STAT3/PDL1 pathway in Lewis lung cancer mice,and explore its mechanism on apoptosis of tumor cells in mice.The mice were randomly divided into four groups:model group,AT-II low,middle and high dose groups(n=10 in each group).0.2 mL of AT-II (25,50,100 mg/kg) was given intragastrically to the low,middle and high dose groups once a day,and the same volume of solvent was given intragastrically to the model group once a day.Twent-four hours after the last administration,the tumor tissues and spleen tissues were separated.The changes of tumor volume,spleen index and tumor growth inhibition rate were observed,and the apoptosis of tumor cells was observed by TUNEL fluorescence staining.The expression of JAK2,p-JAK2,STAT3,p-STAT3 and PDL1 protein was detected by Western blot,and the expression of p-JAK2,p-STAT3,F4/80⁺ and CD206⁺ was detected by immunofluorescence.There was no statistical difference of spleen index in each group (P>0.05).Compared with the model group,the volume and quality of the tumor in the low,middle and high dose groups of atractylodes macrocephala were significantly decreased (P<0.05),the growth inhibition rate was significantly increased,tunel staining showed that compared with the model group,there was no significant difference in apoptosis index in the low dose group (P>0.05),but significantly increased in middle and high dose groups,the results of Western blot showed that the expression of p-JAK2,p-STAT3 and PDL1 in the tumor tissues of the treated group was significantly lower than that of the model group.The levels of p-JAK2,p-STAT3 and CD206⁺ were significantly lower than those of the model group(P<0.01),while the levels of F4/80⁺ were not significantly different (P>0.05).These results suggest that AT-II can modulate the expression of PDL1 based on JAK2/STAT3 pathway and influence tumor cell apoptosis in Lewis lung cancer mice.