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Objective To observe the effect of aerosol inhalation of L-arginine on acute airway inflammation in mice model with asthma and to investigate the mechanism. Methods Thirty male BALB / c mice were randomly divided into three groups and 10 mice in each group: L-arginine group,model group and the control group. The L-arginine group and model group were sensitized by intraperitoneal( i. p.) injections of 0. 3 m L suspension of 100 μg OVA and 2 mg AL( OH)3,and the control group was injected with 0. 3 m L PBS at the same time. Since the 21 st day,these three groups were put into homemade glass atomization box. L-arginine group and model group were given 30 g / L OVA for aerosol inhalation and the control group with PBS for aerosol inhalation,once a day,thirty minutes one time and for 12 days. L-arginine group was given 174 mg / m L L-arginine for aerosol inhalation for 30 minutes before every sensitization. Twenty-four hours after the last sensitization,mice of the three groups were bled to death,and then we collected the left lung tissues and the bronchoalveolar lavage fluid. HE staining was used on the upper left lobe of lung tissue,and the pathological changes were observed. We counted the total number of leukocytes,esosinophils,lymphocytes and macrophages. The levels of interlerkin-4( IL-4),NO and interferon-γ( IFN-γ) in BALF were measured by ELISA. Results In the model group,the airway epithelium fractured, fell off and had mucous edema with more folds under HE staining, and there was inflammatory cell infiltration with a large number of esosinophils and lymphocytes around the bronchus. The inflammatory cell infiltration and mucous edema in the L-arginine group was less than that of the model group. Compared with the control group,the leukocytes, esosinophils, lymphocytes and macrophages in BALF were increased in the L-arginine group and the model group, and the above indexes of the L-arginine group were less than those of the model group( all P 0. 05). Compared with the control group, the levels of IL-4 and IL-4 / IFN-γ were increased, but the levels of IFN-γ and NO were decreased in the Larginine group and model group; compared with the model group, the levels of IL-4 and IL-4 / IFN-γ declined, but IFN-γand NO elevated in the L-arginine group, and significant difference was found among these groups( all P 0. 05). Conclusion The aerosol inhalation of L-arginine can inhibit the airway inflammation of asthmatic mice, and its mechanism may be related to inhibiting IL-4 expression, promoting IFN-γ expression and the production of NO. [ABSTRACT FROM AUTHOR]