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目的:探讨哮喘易感基因ORMDL3在支气管哮喘发病时的表达及地塞米松的干预作用。方法:将30只健康清洁级雌性Balb/c小鼠随机分为3组:对照组、哮喘组(卵蛋白致敏)、地塞米松组(卵蛋白致敏,激发前腹腔注射地塞米松1 mg/kg进行干预),每组10只。称量和观察小鼠的体重增长趋势,对小鼠肺组织进行HE染色评价浸润情况,计数3组小鼠的外周血嗜酸性粒细胞,ELISA法检测对比3组小鼠血清白介素4(IL-4)的浓度变化,采用反转录-聚合酶链反应(RT-PCR)方法检测小鼠肺组织ORMDL3 mRNA水平表达。结果:哮喘组小鼠体重增长显著落后于其他两组(P<0.05),地塞米松干预后能缓解生长迟滞,但仍低于对照组(P<0.05)。病理组织学显示哮喘组小鼠肺组织见大量嗜酸性粒细胞浸润,黏膜下层和平滑肌增厚,管腔狭窄,地塞米松组小鼠肺组织改变较哮喘组为轻。哮喘组外周血嗜酸性粒细胞计数显著高于对照组和地塞米松组(P<0.05),地塞米松组计数高于对照组(P<0.05)。哮喘组小鼠的IL-4水平显著高于对照组(P<0.05),经地塞米松干预后IL-4水平显著降低(P<0.05),但仍高于对照组。哮喘组小鼠ORMDL3 mRNA的表达水平较对照组显著升高,地塞米松组小鼠ORMDL3 mRNA水平较哮喘组下降,但未达统计学意义(P>0.05)。结论:卵清蛋白小鼠哮喘模型中ORMDL3的mRNA表达显著增高,地塞米松可下调ORMDL3的表达,但未达到统计学意义,其中的机制有待进一步的深入研究。
OBJECTIVE: To investigate the expression of ORMDL3, a susceptibility gene of asthma, and the effect of dexamethasone on bronchial asthma. Methods: Thirty healthy and clean female Balb / c mice were randomly divided into three groups: control group, asthma group (ovalbumin sensitization), dexamethasone group (ovalbumin sensitization, pre-challenge intraperitoneal injection of dexamethasone 1 mg / kg for intervention), 10 in each group. Weighing and observing the tendency of body weight gain in mice, HE staining was used to evaluate the infiltration of mouse lung tissue, the peripheral blood eosinophils were counted in 3 groups of mice, ELISA was used to detect the levels of serum interleukin-4 (IL- 4), and the expression of ORMDL3 mRNA in lung tissue of mice was detected by reverse transcription-polymerase chain reaction (RT-PCR). Results: The weight gain of mice in asthma group was significantly lower than that in the other two groups (P <0.05). Dexamethasone could delay the growth retardation but still lower than the control group (P <0.05). Histopathology showed that a large number of eosinophil infiltration, thickening of the submucosa and smooth muscle, stenosis of the lumen were found in the lung tissue of asthmatic mice. The lung tissue of dexamethasone group was lighter than the asthma group. Eosinophil counts in asthmatic group were significantly higher than those in control group and dexamethasone group (P <0.05), dexamethasone group was higher than that in control group (P <0.05). The level of IL-4 in asthmatic mice was significantly higher than that in control group (P <0.05). The level of IL-4 was significantly decreased after dexamethasone intervention (P <0.05), but still higher than that in control group. The expression of ORMDL3 mRNA in asthmatic mice was significantly higher than that in control mice, but the level of ORMDL3 mRNA in dexamethasone mice was lower than that in asthmatic mice (P> 0.05). CONCLUSION: ORMDL3 mRNA expression is significantly increased in ovalbumin-induced mouse asthma model, while dexamethasone can down-regulate the expression of ORMDL3, but the statistical significance has not been reached. The mechanism needs to be further studied.