黄芪甲苷对哮喘模型小鼠气道炎症及IL-22的影响
发布时间：2019-07-01 20:22
【摘要】：目的观察白介素22(IL-22)在哮喘模型中的作用,研究黄芪甲苷(AS-Ⅳ)对哮喘小鼠模型气道炎症及IL-22的调控作用,探讨AS-Ⅳ治疗哮喘的作用机制。方法 32只4周龄BALB/c小鼠随机分为对照组、哮喘组、布地奈德(BUD)组和AS-Ⅳ组4组,用卵清蛋白(OVA)致敏、激发小鼠以制备哮喘模型。小鼠肺组织行HE及ABPAS染色,进行气道炎症评分,ELISA法检测4组小鼠肺泡灌洗液(BALF)中IL-22的水平,实时荧光定量PCR(RTPCR)检测小鼠肺组织中IL-22 mRNA的表达水平,流式细胞术检测小鼠脾单细胞悬液中Th22的比例。结果与对照组相比,哮喘小鼠肺组织炎症评分增加(P0.05),BALF中IL-22水平增高(P0.01),肺组织中IL-22 mRNA表达水平升高(P0.01),脾单细胞悬液中Th22比例增加(P0.01),差异具有统计学意义。给予BUD及AS-Ⅳ治疗后,小鼠气道炎症评分降低(P0.05),IL-22 mRNA的表达水平及Th22细胞的比例均较哮喘组降低(P0.01),差异具有统计学意义。结论 AS-Ⅳ对哮喘气道炎症发挥治疗性作用,这可能与AS-Ⅳ通过抑制Th22细胞分化、抑制IL-22的表达和分泌有关。
[Abstract]:Objective to observe the role of IL-22 (IL-22) in asthma model, to study the regulatory effect of astragalosides (AS- IV) on airway inflammation and IL-22 in asthma mice, and to explore the mechanism of AS- IV in the treatment of asthma. Methods 32 4-week-old BALB/c mice were randomly divided into four groups: control group, asthma group, budesonide (BUD) group and AS- IV group. The mice were sensitized with ovalbumin (OVA) to establish asthma model. HE and ABPAS staining were performed in mouse lung tissue, airway inflammation score was performed. The level of IL-22 in alveolar lavage fluid (BALF) was detected by ELISA method, the expression of IL-22 mRNA in lung tissue was detected by real-time fluorescence quantitative PCR (RTPCR), and the proportion of Th22 in mouse spleen single cell suspension was detected by flow cytometry. Results compared with the control group, the inflammatory score of lung tissue of asthma mice was increased (P 0.05, the level of IL-22 in), BALF was increased (P 0.01), the expression level of IL-22 mRNA in lung tissue was increased (P 0.01), and the proportion of Th22 in spleen single cell suspension was increased (P 0.01), the difference was statistically significant. After treatment with BUD and AS- IV, the score of airway inflammation in mice decreased (P 0.05), the expression level of IL-22 mRNA and the proportion of Th22 cells were lower than those in asthma group (P 0.01), the difference was statistically significant. Conclusion AS- IV plays a therapeutic role in airway inflammation in asthma, which may be related to the inhibition of IL-22 expression and secretion by AS- IV by inhibiting the differentiation of Th22 cells.
【作者单位】： 中国人民解放军空军总医院儿科;
【基金】：空军总医院基金资助项目(KZ2014005)
【分类号】：R285.5;R-332
[Abstract]:Objective to observe the role of IL-22 (IL-22) in asthma model, to study the regulatory effect of astragalosides (AS- IV) on airway inflammation and IL-22 in asthma mice, and to explore the mechanism of AS- IV in the treatment of asthma. Methods 32 4-week-old BALB/c mice were randomly divided into four groups: control group, asthma group, budesonide (BUD) group and AS- IV group. The mice were sensitized with ovalbumin (OVA) to establish asthma model. HE and ABPAS staining were performed in mouse lung tissue, airway inflammation score was performed. The level of IL-22 in alveolar lavage fluid (BALF) was detected by ELISA method, the expression of IL-22 mRNA in lung tissue was detected by real-time fluorescence quantitative PCR (RTPCR), and the proportion of Th22 in mouse spleen single cell suspension was detected by flow cytometry. Results compared with the control group, the inflammatory score of lung tissue of asthma mice was increased (P 0.05, the level of IL-22 in), BALF was increased (P 0.01), the expression level of IL-22 mRNA in lung tissue was increased (P 0.01), and the proportion of Th22 in spleen single cell suspension was increased (P 0.01), the difference was statistically significant. After treatment with BUD and AS- IV, the score of airway inflammation in mice decreased (P 0.05), the expression level of IL-22 mRNA and the proportion of Th22 cells were lower than those in asthma group (P 0.01), the difference was statistically significant. Conclusion AS- IV plays a therapeutic role in airway inflammation in asthma, which may be related to the inhibition of IL-22 expression and secretion by AS- IV by inhibiting the differentiation of Th22 cells.
【作者单位】： 中国人民解放军空军总医院儿科;
【基金】：空军总医院基金资助项目(KZ2014005)
【分类号】：R285.5;R-332
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