黃芪甲苷對哮喘模型小鼠氣道炎癥及IL-22的影響
發(fā)布時間：2019-07-01 20:22
【摘要】：目的觀察白介素22(IL-22)在哮喘模型中的作用,研究黃芪甲苷(AS-Ⅳ)對哮喘小鼠模型氣道炎癥及IL-22的調(diào)控作用,探討AS-Ⅳ治療哮喘的作用機制。方法 32只4周齡BALB/c小鼠隨機分為對照組、哮喘組、布地奈德(BUD)組和AS-Ⅳ組4組,用卵清蛋白(OVA)致敏、激發(fā)小鼠以制備哮喘模型。小鼠肺組織行HE及ABPAS染色,進行氣道炎癥評分,ELISA法檢測4組小鼠肺泡灌洗液(BALF)中IL-22的水平,實時熒光定量PCR(RTPCR)檢測小鼠肺組織中IL-22 mRNA的表達水平,流式細胞術(shù)檢測小鼠脾單細胞懸液中Th22的比例。結(jié)果與對照組相比,哮喘小鼠肺組織炎癥評分增加(P0.05),BALF中IL-22水平增高(P0.01),肺組織中IL-22 mRNA表達水平升高(P0.01),脾單細胞懸液中Th22比例增加(P0.01),差異具有統(tǒng)計學(xué)意義。給予BUD及AS-Ⅳ治療后,小鼠氣道炎癥評分降低(P0.05),IL-22 mRNA的表達水平及Th22細胞的比例均較哮喘組降低(P0.01),差異具有統(tǒng)計學(xué)意義。結(jié)論 AS-Ⅳ對哮喘氣道炎癥發(fā)揮治療性作用,這可能與AS-Ⅳ通過抑制Th22細胞分化、抑制IL-22的表達和分泌有關(guān)。
[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.
【作者單位】： 中國人民解放軍空軍總醫(yī)院兒科;
【基金】：空軍總醫(yī)院基金資助項目(KZ2014005)
【分類號】：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.
【作者單位】： 中國人民解放軍空軍總醫(yī)院兒科;
【基金】：空軍總醫(yī)院基金資助項目(KZ2014005)
【分類號】：R285.5;R-332
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