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目的研究皮质类固醇激素调节小鼠哮喘模型树突细胞表面共刺激分子表达的机制,以及肺表面活性蛋白A(SP-A)在其调节中的作用。方法BALB/c小鼠30只,分为3组:哮喘组,采用卵蛋白(OVA)致敏和激发;对照组,以生理盐水代替OVA;治疗组,每次OVA激发后10min,腹腔注射地塞米松0·1mg。用免疫组化法检测SP-A在肺内的表达情况。采用LeicaDMSnk软件进行图像采集,并用Qwin软件计算小气道内棕色区域面积,取平均值,进行统计分析。分离培养脾脏树突细胞,用流式细胞仪(FACS)检测树突细胞表面共刺激分子CD80的表达变化。结果哮喘组肺组织表现为嗜酸性细胞及淋巴细胞浸润为主的炎症变化,治疗组和对照组无此变化。哮喘组的SP-A表达明显低于对照组和治疗组(P<0·01),CD80的表达率明显高于治疗组(P<0·01);哮喘组小气道内SP-A表达与树突细胞CD80阳性率呈负相关(r=-0·907,P<0·01)。结论皮质类固醇对小鼠哮喘模型的肺表面活性蛋白有明显的保护作用,可通过激发肺表面活性蛋白抑制树突细胞表面共刺激分子CD80的表达。
Objective To investigate the mechanism of cortical steroid hormone regulating the expression of costimulatory molecules on dendritic cells of mouse asthma model and the role of pulmonary surfactant protein A (SP-A) in its regulation. Methods Thirty BALB / c mice were randomly divided into three groups: asthma group, sensitized and challenged with ovalbumin (OVA); control group, normal saline instead of OVA; treatment group, each OVA challenge 10min, Mismatch 0 · 1mg. The expression of SP-A in lungs was detected by immunohistochemistry. Using LeicaDMSnk software for image acquisition, and using Qwin software to calculate the area of small airway brown area, take the average, for statistical analysis. The spleen dendritic cells were isolated and cultured. The expression of costimulatory molecule CD80 on dendritic cells was detected by flow cytometry (FACS). Results The lung tissue of asthmatic group showed inflammatory changes of eosinophil and lymphocyte infiltration. There was no change in the treatment group and the control group. The expression of SP-A in asthma group was significantly lower than that in control group and treatment group (P <0.01), and the expression of CD80 was significantly higher in asthma group than in treatment group (P <0.01) The positive rate of CD80 was negatively correlated (r = -0.0907, P <0.01). Conclusions Corticosteroids have a significant protective effect on pulmonary surfactant protein in mouse asthma model, which can inhibit the expression of costimulatory molecule CD80 on the surface of dendritic cells by activating pulmonary surfactant protein.