目的  探讨布地奈德（BUD）吸入对哮喘大鼠气道平滑肌细胞（ASMCs）增殖、凋亡的影响及其分子生物学机制。   方法  40只SD大鼠随机分为对照组、哮喘模型组、BUD低及高剂量（0.25 mg/kg、2 mg/kg）组，采用卵蛋白（VOA）联合氢氧化铝凝胶致敏激发构建大鼠哮喘模型，干预组在致敏后激发前雾化吸入不同剂量BUD。采用医学图像分析系统测定并计算各组大鼠肺组织气道相关参数；采用免疫荧光检测大鼠气道平滑肌（ASM）组织中Ⅰ型（ColⅠ）和Ⅲ型胶原蛋白（Col Ⅲ）的表达；Western blotting检测大鼠ASM组织中Bcl-2、Bax、Caspase-3、磷酸化ERK 1/2（p-ERK 1/2）及p-p38 MAPK蛋白表达。组织贴壁法分离培养原代ASMCs，采用MTT法检测ASMCs增殖活性；流式细胞术检测ASMCs凋亡率。   结果  与对照组比较，哮喘模型组大鼠气道发生重塑，气道总管壁厚度（WAt/Pbm）、内壁厚度（WAi/Pbm）和平滑肌厚度（WAm/Pbm）增加；与模型组比较，BUD干预组大鼠气道重塑被抑制，气管WAt/Pbm、WAi/Pbm和WAm/Pbm均降低；BUD能降低哮喘大鼠ASMCs增殖活性，提高ASMCs凋亡率，抑制哮喘大鼠ASM组织ColⅠ、Col Ⅲ的表达，下调哮喘大鼠ASM组织Bcl-2蛋白表达，上调Bax、Caspase-3蛋白表达（均P<0.05），抑制ERK 1/2、p38 MAPK信号通路的活性。   结论  BUD可抑制哮喘大鼠ASMCs增殖，并促进其凋亡，可能机制与抑制ERK 1/2及p38 MAPK信号通路有关。

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.