摘要
目的观察地塞米松对小鼠哮喘模型气道炎症和肺组织CC型趋化因子Eotaxin和受体CCR3表达的影响。方法建立哮喘模型,自第14天雾化吸入OVA前0.5h,干预组分别雾化吸入咪喹莫特30min及ip地塞米松。OVA雾化结束后24h,每组小鼠眼球摘除采血收集血清。采用酶联免疫吸附法测定血清、支气管肺泡灌洗液及肺组织匀浆中Eotaxin水平:收集肺泡灌洗液进行细胞计数和分类;H-E染色观察肺组织炎症改变;用免疫组化方法检测肺组织Eotaxin和CCR3的表达;用Westernblot方法测定肺组织CCR3表达;用逆转录-聚合酶链反应半定量检测肺组织IL-4、IFN-γ、Eotaxin、和CCR3mRNA表达水平。结果H-E染色可见地塞米松组小鼠气道炎症程度减轻;地塞米松治疗组嗜酸性粒细胞、单核细胞和淋巴细胞比哮喘组明显减少;哮喘组小鼠血清和肺组织匀浆Eotaxin水平较正常组升高,地塞米松治疗组小鼠较哮喘组下降;Eotaxin、CCR3均在气道上皮细胞表达,哮喘组小鼠气道上皮细胞Eotaxin、CCR3较正常组增加,地塞米松治疗组较哮喘组减轻;哮喘组小鼠肺组织EotaxinCCR3和IL-4mRNA表达较正常组增强,地塞米松治疗组小鼠肺组织Eotaxin、CCR3和IL-4mRNA表达较哮喘组降低。结论地塞米松减轻哮喘小鼠的气道炎症与抑制哮喘小鼠肺组织Eotaxin、CCR3蛋白和mRNA的过度表达有关。
[Objective] To observe the effects of dexamethasone on the antigen-lnduced airway inflammation and the expression of CC cheomokine Eotaxin and its receptor CCR3 in mouse asthma models. [Methods ] The mouse asthma models （asthma group） were established by sensitization and challenge with ova]bumin （OVA）, ten mice were administrated dexamethasone by injection abdomenly 30 min before challenge （dexamethasone group）, the healthy control mice were treated with normal saline instead of OVA. Serum were collected 24 h after the last challenge. bronchoalveolar lavage （BAL） was performed, total cell counts, cell sorts were examined. The levels of Eotaxin in serum,BALF and lung homogenate were measured by ELISA. The expression of Eotaxin and CCR3 in lung were detected by immunohistoehemistry. The expression of Eotaxin and CCR3 in lung were also detected by ELISA and Western blot separately. The mRNA expression of Eotaxin, CCR3 IL-4 and IFN-γ in lung were examined by reverse transcript-polymerase chain reaction. [Results] The Eotatin levels of serum and lung homogenate in asthma group were significantly different from those in control group （P 〈0.01） and dexamethasone group （P 〈0.05）. Total cell counts, EOS and lymphocyte in BALf of asthma group were increased significantly. Dexamethasone can decrease the totol cell counts, EOS and lymphocyte counts in BALf. The expression of Eotaxin and CCR3 was mainly on the bronchial epithelium, The expression of Eoaxin and CCR3 of dexamethasonc group was decreased compared with asthma group. The Eotaxin, CCR3 and IL-4 mRNA expression of lung in asthma group had significant differences from those in control group （P 〈0.01） and those in dexamethasone （P 〈0.05） group as well. [Conclusion] The experiment dates suggest that dexamethasone inhibits antigen-induced airway inflammation by decreasing the protein and mRNA expression of CC chemokine Eotaxin and its receptor CCR3 in mouse asthma models.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2006年第8期1140-1144,1148,共6页
China Journal of Modern Medicine
