Objective To investigate the effect of honokiol (HNK) on immune imbalance and lung function in chronic obstructive pulmonary disease (COPD) mice and to investigate whether the Notch signaling pathway mediates this process. Methods BALB/ c mice (male, 6~ 8 weeks old) were randomly divided into three groups: normal control group (Normal), COPD group and COPD+HNK group ( n= 10 mice per group). A mouse model of COPD was induced by cigarette smoke, and HNK (10 mg / kg) was intraperitoneally injected into the COPD+HNK group every other day for 30 days. The French EMKA GYD-003 animal lung function test system was used to detect the peak inspiratory flow rate (PIF) and peak expiratory flow rate (PEF). Hematoxylin-eosin (HE) staining was used to evaluate the pathological changes of lung tissue. Flow cytometry was used to detect the ratio of Th1 / Th2 and Th17 / Treg subgroups of mouse spleen T cells. Western blot was used to examine the protein expression of Notch 1 / 2 / 3 / 4, Hes1, Hes5 and Hey1 in T cells. ELISA was used to detect the levels of serum IFN-γ, IL-4, IL-17 and IL-10 in mice. Results The PIF and PEF of the COPD+HNK group mice were significantly increased compared with result in the COPD group (P<0. 05). In addition, the lung tissue lesions of the mice in the COPD+HNK group were reduced, the inflammatory cell infiltration was reduced, the number of alveoli increased and the alveolar cavity was reduced compared with result in the COPD group. Compared with the COPD group, the COPD+HNK group mice showed significantly reduced Th1 percentage, Th1 / Th2 ratio, Th17 percentage and Th17 / Treg ratio (P<0. 05). In addition, the relative expression levels of Notch1, Notch2, Notch3, Notch4, Hes1, Hes5 and Hey1 in the spleen T cells of the COPD+HNK group mice were significantly reduced (P<0. 05). The levels of IFN-γ and IL-17 in the serum of the COPD+HNK group were significantly reduced (P<0. 05), while the levels of IL-4 and IL-10 were significantly increased (P<0. 05). Conclusions HNK inhibits activation of the Notch signaling pathway of T cells in the spleen of COPD mice, thereby correcting the imbalance of Th1 / Th2 and Th17 / Treg cells in COPD mice and improving lung function.