外感温燥咳喘病机的实验研究

目的:研究温燥对气道组织结构与功能、黏液素基因(MUC5ac)表达和核因子NF-κB活性等影响。方法:138只SPF级昆明种小鼠随机分为常温常湿组、常温燥组、温燥组,每组46只。于处理后第6天与第12天行气管与肺组织超微结构观察、MUC5ac表达、NF-κB活性、气管纤毛运动(CM)、气道液黏多糖(MS)、IgG与分泌型IgA(SIgA)及二棕榈酰卵磷酯(DPPC)含量的影响。结果:与常温常湿组比较,常温燥组第6天、第12天气道组织改变不明显;温燥组气管上皮细胞鳞状化生与纤毛缺损、腺体化生伴炎性细胞浸润,肺泡瘀血伴肺气肿,超微结构显示Ⅱ型肺泡细胞(ATⅡ)嗜锇板层小体数量减少与线粒体肿胀;温燥组CM加快、MUC5a mRNA表达上调但NF-κB活性下降、RM、IgG、SIgA与DP-PC下降(P<0.01)。结论:温燥袭肺使受邪部位津液骤伤、抗体含量下降和削弱"纤毛-黏液毯"御邪之功,MUC5ac基因表达上调和NF-κB活性受抑可致ATⅡ分泌肺泡表面活性物质功能障碍而损调节肺通气之功,肺失输布则炎性之物聚而为痰致病,结果为温燥之"痰、咳、喘"诸证提供实验证据。

Experimental Study on Pathological Mechanism of Cough and Asthma Due to Warm Dryness

Objective:To investigate the influence on the structures and functions of the airway,expression of MUC 5ac and activation of NF-κB.Methods:138 Kuming mice(SPF)were randomly divided into the normal-temperature and normal-dampness group(group A),normal-temperature and dryness group(group B),warm-dryness group(group C),46 mice in each group.The mice model was established with the documents.After 6,12 days the histopathological changes of airway,MUC5ac expression and NF-κB activation,mucopolysaccharide(RM),cilia movement(CM),IgG and secretory IgA(SIgA)and Dipalmitoyl Phosphatidyl Choline(DPPC)were detected respectively.Results:Compared with group A,the changes in airway were not obvious in group B.In the group C there was squamous metaplasia of airway epithetlium and injury of the cilium,and metaplasia of the serous gland as infiltrating of inflammatory cells and congested and dropsied of pulmonary alveolus;the number of Osmiophilic Multilamellar Body in typeⅡalveolar epithelial cell(ATⅡ)was reduced and swelled of Mitochondrion;as speeding of CM and increase of MUC5ac mRNA but restrained of NF-κB activation and decreased of RM,IgG and SIgA and DPPC(P<0.01)in days 6~12 were significant.Conclusion:The result suggested the evidence for sputum,cough and asthma due to warm dryness that can induce the impairment of the airway,exhaust the lung-fluid,weaken the antibodies and damage the cilia-mucus barrier,and the pulmonary ventilation was disordered due to damage of the surfactant synthesis of ATⅡ and,the increase of MUC5ac expression and restrained of NF-κB activation and the inflammatory fluids turned to the sputum-evils.