Objective  To investigate the effect of budesonide (BUD) inhalation on the proliferation and apoptosis of airway smooth muscle cells (ASMCs) in asthmatic rats and its molecular biological mechanism.    Methods  Totally 40 SD rats were randomly divided into control group, asthma model group, low (0.25 mg/kg) and high (2 mg/kg) BUD group . The rat asthma model was induced by ovalbumin (VOA) combined with aluminium hydroxide Gel sensitization stimulation. After sensitization, the intervention group inhaled different doses of BUD before stimulation. The related parameters of lung tissue and airway were measured and calculated by medical image analysis system, immunofluorescence was used to detect the expression of type Ⅰ collagen（Col Ⅰ）and Col Ⅲ in rat airway smooth muscle (ASM), and the protein expressions of Bcl-2, Bax, Caspase-3, phosphorylated ERK 1 and 2（p-ERK 1 / 2）, p-p38 MAPK were detected by Western blotting. The proliferation activity of ASMCs was detected by MTT method , and the apoptosis rate of ASMCs was detected by flow cytometry.   Results  Compared with the control group, airway remodeling occurred in the asthmatic model group, and the airway wall thickness (WAt/Pbm), inner wall thickness (WAi/Pbm) and smooth muscle thickness (WAm/Pbm) increased, compared with the model group, the airway remodeling was inhibited in BUD intervention group, and the tracheal WAt/Pbm, WAi/Pbm and WAm/Pbm decreased in bud treatment group. BUD could decrease the proliferation activity of ASMCs, increase the apoptosis rate of ASMCs, inhibit the expression of Col Ⅰ and Col Ⅲ, deregulate the expression of Bcl-2, upregulate the expression of Bax and Caspase-3 (all  P<0.05), and inhibit the activity of ERK 1/2 and p38 MAPK signal pathway.    Conclusion  BUD can inhibit the proliferation and the promote apoptosis of ASMCs in asthmatic rats, which may be related to the inhibition of ERK 1/2 and p38 MAPK signal pathways.