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目的探讨miR-33a在哮喘患儿及哮喘小鼠中的表达及其对气道炎症的作用。方法应用real-time PCR方法检测哮喘患儿和健康儿童痰液,以及卵清蛋白诱导的哮喘小鼠和正常小鼠肺组织中miR-33a的表达;化学合成miR-33a模拟物与阴性对照,并分别鼻滴至哮喘小鼠,HE染色验证哮喘小鼠模型的成功建立,免疫荧光方法和Western blot方法检测各组小鼠肺组织肿瘤坏死因子-α(TNF-α)与白介素-6(IL-6)的蛋白表达。结果与对照组相比,哮喘患儿痰液及哮喘小鼠肺组织中miR-33a表达显著降低(P<0.01);HE染色显示哮喘模型组小鼠炎症细胞浸润明显高于正常对照组,哮喘小鼠模型成功建立。miR-33a模拟物滴入后,哮喘小鼠肺组织TNF-α与IL-6的蛋白表达显著降低(P<0.01)。结论 miR-33a在支气管哮喘患儿及支气管哮喘小鼠模型中低表达,miR-33a模拟物能够抑制哮喘小鼠的气道炎症。
Objective To investigate the expression of miR-33a in asthmatic children and asthmatic mice and its effect on airway inflammation. Methods Real-time PCR method was used to detect the expression of miR-33a in the sputum of asthmatic children and healthy children as well as the ovalbumin-induced asthmatic mice and normal mice. Chemosynthesis of miR-33a mimics and negative controls, The mice were killed by intranasal injection of rhBMP-2, and were respectively nasally dripped into asthmatic mice. HE staining was used to establish a mouse model of asthma. Immunofluorescence and Western blot were used to detect the expressions of tumor necrosis factor-α (TNF-α) and interleukin-6 -6) protein expression. Results Compared with the control group, the expression of miR-33a in sputum and asthmatic mice lungs was significantly decreased (P <0.01). The HE staining showed that the infiltration of inflammatory cells in the asthmatic model group was significantly higher than that in the normal control group and asthma Mouse model was successfully established. After miR-33a mimics dripped, the protein expression of TNF-α and IL-6 in lung tissue of asthmatic mice decreased significantly (P <0.01). Conclusion miR-33a is overexpressed in asthmatic mice and bronchial asthma mouse models. MiR-33a mimics can inhibit airway inflammation in asthmatic mice.