Objective：To establish a C57bl/6 mouse asthma model the ovalbumin（OVA） free and to evaluate the model using dexam－ethasone（Dex）. Methods：Clean female C57bl/6 mice fed without OVA for over 3 generations were divided into three groups（n=36，12 for each group）. The asthmatic group was sensitized by i.p with OVA aluminium hydroxide gel on day 1 and 14. From 21st day，asthmatic group was aerosolized 1.5% OVA for 7 days. The control group received saline as the substitution of OVA. The treated group was i.p with 5 mg/kg dexamethasone 0.5 h before atomization from 25th to 27th day. Twenty four hour after last atomization，6 mice in each group were used to detect the airway resistance by invasive pulmonary function. The last 6 mice were used to detect airway in－flammatory cells，lung pathological changes，mucus hypersecretion，total IgE in serum and IL-4 by bronchoalveolar lavage fluid（BALF），hematoxylin-eosin（HE） staining，periodic acid-schiff（PAS） staining and ELISA. Results：The airway resistance lung resistant in asthma group was higher than that in control group at 25 mg/mL concentration（F=26.530，P=0.000） and also higher than that in control group at 50 mg/mL concentration（F=18.690，P=0.000）. BALF total cells of asthma group were higher than that in control group（F=1.349，P=0.000） and treatment group（F=1.461，P=0.006）. The eosinophils cells of asthma group was higher than that of control group（F=7.000，P=0.013）. Lung pathological changes and mucus hypersecretion in asthma group were much serious. Total IgE in serum（F=15.10，P=0.036） and IL-4 in BAlF（F=15.10，P=0.036） of asthma group were more serious than those of control group. Conclusion：The C57bl/6 mouse allergic asthma model is es－tablished by the way in this study.