黄芪甲苷对哮喘模型小鼠气道炎症及IL-22的影响

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AB-PAS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(RT-PCR)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(P<0.05),BALF中IL-22水平增高(P<0.01),肺组织中IL-22 mRNA表达水平升高(P<0.01),脾单细胞悬液中Th22比例增加(P<0.01),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(P<0.05),IL-22 mRNA的表达水平及Th22细胞的比例均较哮喘组降低(P<0.01),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.%Objective To study the role of interleukin-22 (IL-22) in murine asthmatic airway inflammation and airway models, and explore the mechanism of astragaioside (AS) Ⅳin the treatment of asthma.Methods Ovalbumin(OVA) was used as an allergen to sensitize and challenge the mice .Thirty-two female specific-free ( SPF) four-week BALB/c mice were randomly divided into 4 groups:control group , asthma group , budesonide treatment group ( BUD group ) and AS-Ⅳgroup.HE staining and AB-PAS were used to measure the inflammation scores and goblet cells hyperplasia , enzyme-linked immunosorbent assay(ELISA) was used to analyze IL-22 levels in bronchoalveolar lavage fluid (BALF), flow cytometry was performed to analyze the proportion of Th22 cells in spleen single cell suspension , and realtime-PCR was performed to analyze the IL-22 mRNA levels in lung tissue .Results The inflammation scores of asthma group were elevated compared with the control group(P<0.05).An overall reduction of asthmatic airway inflammation was observed in the BUD group and AS-Ⅳgroup by the end of the trial .IL-22 levels in BALF and the proportion of Th22 cells in spleen single cell suspension were significantly increased after treatment in BUD and AS-Ⅳ groups(P<0.01), while the mRNA levels of IL-22 were obviously decreased(P<0.01).Conclusion The increase of IL-22 can induce airway inflammation of asthma . AS-Ⅳcan reduce Th22 cell differentiation and the expression of IL-22, thereby inhibiting the development of airway inflammation of asthma.