中药小青龙汤对哮喘气道平滑肌细胞周期调控机制的影响

目的探讨中药小青龙汤对哮喘气道重构时气道平滑肌细胞（ASMC）增殖周期的调控机制,为哮喘的防治提供新的思路。方法SD大鼠随机分成正常对照组、哮喘模型组和小青龙汤组,每组20只。各组大鼠支气管-肺组织行HE染色和天狼猩红染色,经光学显微镜和图像分析系统观察分析支气管内管壁、气道平滑肌层和上皮下胶原的病理改变,应用流式细胞仪同步检测各组大鼠ASMC增殖周期时相分布和相应细胞周期调节蛋白（CCRP）的表达水平。结果哮喘模型组大鼠支气管内管壁、平滑肌层、上皮下胶原层的厚度和ASMC数目均显著大于正常对照组（P〈0.01）;S期、G2/M期ASMC比例显著高于正常对照组（P〈0.01）,cyclinE、cyclinA、cyclinB表达水平显著高于正常对照组（P〈0.01）,P27kip1表达水平显著低于正常对照组（P〈0.01）。小青龙汤组大鼠支气管内管壁、平滑肌层、上皮下胶原层的厚度和ASMC数目均显著小于哮喘模型组（P〈0.05）,S期ASMC比例显著低于哮喘模型组（P〈0.05）,cyclinE、cyclinA表达水平显著低于哮喘模型组（P〈0.05）,P27kip1表达水平显著高于哮喘模型组（P〈0.05）。结论哮喘气道重构时ASMC异常增殖,小青龙汤可通过调控CCRP的表达、影响ASMC通过G1/S细胞周期限制点而抑

Effect of Xiaoqinglong decoction on the regulation of the cell cycle of airway smooth muscle cells in asthmatic rats

Objective To investigate the effect of Xiaoqinglong Decoction(XQLD) on the cell cycle of airway smooth muscle cell(ASMC) in asthmatic rats with airway remodeling and explore a new method for prevention and treatment of asthma.Methods SD rats were divided randomly into control group,asthma group and XQLD group(20 rats in each group).The pathologic changes of inner airway wall,airway smooth muscle cells and subepithelial collagen fiber of the rats were determined by observing and analyzing the lung tissue sections stained with HE and Cirius red.Cell cycle distribution and expression of cell cycle regulatory protein(CCRP) of ASMC were analyzed by flow cytometry.Results The inner airway wall,smooth muscle layer and subepithelial collagen fiber were much thicker in rats of asthma group than those in control group(P<0.01).The percentage of ASMC in the S phase and G2/M phase in asthma group was significantly higher than those in control group(P<0.01).The expression of cyclinE,cyclinA,cyclinB of ASMC in asthma group were significantly higher than those in control group(P<0.01),and the expression of P27kip1of ASMC in asthma group was significantly lower than that in control group(P<0.01).The inner airway wall,smooth muscle layer and subepithelial collagen fiber were much thinner in rats of XQLD group than those in asthma group(P<0.05).The percentage of ASMC in S phase in XQLD group was significantly lower than that in asthma group(P<0.05).The expression of cyclinE,cyclinA of ASMC in XQLD group were significantly lower than those in asthma group(P<0.05),and the expression of P27kip1of ASMC in XQLD group was significantly higher than that in asthma group(P<0.05).Conclusions The ASMC were in excessive proliferation in asthmatic rats with airway remodeling.XQLD may prevent airway remodeling and suppress proliferation of ASMC by G1/S checkpoint arrest via regulating the expression of CCRP.