Objective：To study the influence on pulmonary fibrosis and expression of Bax/Bcl-2 in the lung after blocking interleukin（IL）-17 activity in mice induced by bleomycin（BLM）. Methods：A total of 80 C57BL/6 mice were randomly divided into the following 4 groups，including the model group treated with neutralizing IL-17 antibody，the model group treated with isotype-matched control antibody，the model group and the PBS group. The three model groups were received a single intratracheal instillation of 5 mg/kg body weight of BLM in 0.05 mL sterile saline，while the PBS group were administrated the equivalent sterile saline. All mice were injected from the caudal vein with neutralizing rat antimouse IL-17 mAb，or control rat IgG，or PBS alone every 3 d starting on d1 before making models. At 28 d after model establishment，lung tissues from all mice were removed and used to measure the extent of pulmonary fibrosis by Masson staining and hydroxyproline contents measurement. The apoptosis rate of pulmonary cells was detected by flow cytometry（FCM）. Meanwhile，the expressions of Bax/Bcl-2 in mice were also evaluated by immunohistochemistry（IHC）. Results：Compared with other groups，the pulmonary fibrosis degree，hydroxyproline contents and apoptosis rate were significantly decreased in mice blocked with anti-IL-17 mAb（P < 0.01，respectively）. Bax protein expression was decreased obviously（P < 0.01），although the Bcl-2 protein expression had no obvious changes，but the ratio of Bax/Bcl-2 decreased significantly（P < 0.01）. Conclusion：Pulmonary fibrosis had been improved significantly after the endogenous IL-17 activity of mice blocked，the apoptosis rate and the ratio of Bax/Bcl-2 were all decreased in lung tissues. These data suggested that IL-17 improving the pulmonary fibrosis induced by BLM may be associated with Bax/Bcl-2 mediated mitochondrial apoptotic pathways.