支气管哮喘的分子机制及地塞米松联合平喘灵的干预作用

目的探讨卵蛋白诱发哮喘模型大鼠血内皮素（ET）、降钙素基因相关肽（CGRP）及肺表面活性物（PS）的变化，以及激素与传统中药平喘灵的调节效应。方法用卵蛋白雾化吸入致敏法，复制大鼠哮喘模型；将SD大鼠分为空白对照组、哮喘模型组、地塞米松组、平喘灵组及小剂量地塞米松＋平喘灵组，共5组。采用免疫放射法、电子显微镜等分别检测各组大鼠cGRP、ET、PS的变化。结果模型组cGRP、ET的含量均较空白组明显升高（P〈0．05），PS及肺泡Ⅱ型上皮细胞结构受损。地塞米松组和小剂量地塞米松＋平喘灵组cGRP、ET的含量较模型组明显降低（P〈0．05），Ps及肺泡Ⅱ型上皮细胞结构异常改变减轻。且小剂量地塞米松＋平喘灵组较单纯平喘灵组较单纯平喘灵组作用明显（P〈0．05）。结论Ps、cGRP、ET的异常表达在大鼠哮喘的发生发展中发挥着重要作用，地塞米松组和小剂量地塞米松＋平喘灵可通过作用于PS、cGRP、ET而发挥治疗哮喘的作用，且平喘灵与激素具有协同效应。

Molecular mechanism of bronchus asthma and the interference effect of dexamethasone with Pingchuanling

Objective To investigate the changes of pulmonary surfactant(PS), gene related peptide(cGRP),endothelin(ET) in ovalbumin-induced asthma rats and the interference effect of dexamethasone with Pingchuanling(PCL).Methods The rats of asthma model was established by ovalbumin(OVA) sensitization.The SD rats were divided into normal group,asthma model group,dexamethasone group,PCL group,low dose dexamethasone + PCL group.cGRP and ET changes in serum were examined with immunoradiometricassay(IRMA).The ultrastructure of PS was observed with electron microscope histochemistry method.Results The cGRP and ET levels in serum of asthma model group increased significantly than those of control group(P<0.05).The ultrastructure of PS was obviously abnormal in asthma group.After be treated with dexamethasone or low dose dexamethasone + PCL,cGRP and ET levels in serum decreased significantly than those of the asthma model group(P<0.05),and ultrastructure change in PS reduced after asthma attack too.Low dose dexamethasone + PCL had more significant effect than PCL(P<0.05).Conclusions The abnormal expression of PS,cGRP and ET could play the important role in attack of asthma in rats.Dexamethasone or low dose dexamethasone + PCL could bring into play to treat asthma through their effect on PS,cGRP and ET having the synergistic with PCL.