Objective：To investigate the effects and the possible mechanism of inhaling budesonid in treating bleomycin-induced pul－monary fibrosis in rats. Methods：Forty-five SD rats were randomly divided into three groups（15 in each group）：control group，model group and intervention group. Rats in intervention group inhaled budesonid every two days from the 7th d after intratracheal instilla－tion while those in model group and control group inhaled the same volume of 0.9% normal saline. Five rats in each group were ran－domly killed on the 7th，14th，28th d after atomizing inhalation and the pulmonary tissues were preserved respectively. HE and Masson staining were used to determine the extent of alveolus inflammation and pulmonary fibrosis. Immunohistochemical technique was used to evaluate the level of transforming growth factor-β（TGF-β） and connective tissue growth factor（CTGF） in lung tissues. RT-PCR was used to detect the level of type Ⅰ and Ⅲ collagen in pulmonary tissues. Results：Pulmonary tissue pathology showed that the ex－tent of alveolus inflammation and pulmonary fibrosis was less intense in control group than in model group and intervention group and was better in intervention group than in model group. Significant over-expressions of CTGF and TGF-β were shown in pulmonary tissues of rats in model group and intervention group（higher expressions in model group than in intervention group，P<0.05） compared with those in control group（P<0.05）. Expressions of type Ⅰ and Ⅲ collagen were significantly higher in model group than in con－trol group（P<0.05），but lower in intervention group than in model group（P<0.05）. Conclusion：Budesonid has anti-fibrosis po－tency，the mechanism of which may be reducing the production of type Ⅰ and Ⅲ collangen through inhibiting the expressions of cy－tokines such as TGF-β and CTGF．