SDF-1 在哮喘大鼠肺组织中的表达及 AMD3100 的干预作用

Expression of SDF-1 in lung tissues and intervention of AMD3100 in asthmatic rats

摘要:

目的：探讨基质细胞衍生因子-1（SDF-1）在哮喘大鼠肺组织中的表达及其拮抗剂AMD3100的干预作用。方法：30 只雌性 Sprague-Dawley 大鼠随机分为对照组、哮喘组、干预组，以卵白蛋白激发制备哮喘模型；干预组于激发前 30 min给予 AMD3100 (50 μg, 隔日 1 次，共 10 次)。光镜下观察各组气道炎症及气道壁结构的情况；酶联免疫吸附法测定肺组织匀浆中 IL-4、IL-5 的水平；RT-PCR 检测 SDF-1 mRNA 在肺组织中的表达。结果哮喘组气道壁厚度较对照组及干预组显著增厚（P<0.05）；干预组IL-4、IL-5 的水平明显低于哮喘组（P<0.05）；哮喘组中SDF-1 mRNA 明显高于对照组及干预组(P<0.05)。结论：SDF-1可能参与哮喘大鼠气道炎症反应和气道重塑过程；AMD3100 能够改善哮喘大鼠的气道炎症和气道重塑，可能与拮抗 SDF-1 的生物活性有关。

Abstract:

OBJECTIVE: To study the expression of stromal cell derived factor-1(SDF-1) in the airway and to investigate the role of SDF-1 receptor antagonist AMD3100 intervention in rats with asthma. METHODS: Thirty Sprague-Dawley rats were randomly divided into three groups: normal control and asthma with and without AMD3100 intervention. The rat model of asthma was prepared by aerosolized ovalbum (OVA) challenge. The AMD3100 intervention group was administered with AMD3100 of 50 μg 30 minutes before challenge every other day, for 10 times. The characteristic airway inflammation and alterations of airway structures were observed by hemetoxylin and eosin staining. The levels of interleukin 4 and interleukin 5 in whole lung homogenates were measured using ELISA. RT-PCR was used to evaluate the expression of SDF-1 mRNA in the lung. RESULTS: The airway wall thickness in the untreated asthma group was greater than that in the control and the AMD3100 intervention groups (P<0.05). The levels of interleukin 4 and interleukin 5 in whole lung homogenates in the AMD3100 intervention group were lower than those in the untreated asthma group (P<0.05). The expression of SDF-1 mRNA in the untreated asthma group was higher than that in the control and the AMD3100 intervention groups (P<0.05). CONCLUSIONS: SDF-1 may be associated with airway inflammation and remodeling in rats with asthma. AMD3100 may reduce the airway inflammation and improve airway remodeling by inhibiting the bioactivity of SDF-1.