黄芪多糖对哮喘小鼠气道重构的干预作用

目的：探讨黄芪多糖（astragalus polysaccharide,APS）对哮喘小鼠气道重构的干预作用。方法：60只4～6周龄SPF（Specific PathogenFree）级BALB/c小鼠,随机均分为对照组、哮喘组、APS治疗组和地塞米松（dexamethasone,DXM）阳性对照组;用卵蛋白（ovalbumin,OVA）致敏/激发哮喘;APS治疗组和DXM阳性对照组分别用APS和DXM肌肉注射治疗。采用二步法免疫组化技术对小鼠肺组织α平滑肌肌动蛋白（smooth muscle actin-α,α-SMA）表达进行检测,采用计算机图像分析系统对气道重塑进行分析。结果：与对照组对比,哮喘组小鼠肺泡灌洗液（bronchoalveolar lavage fliud,BALF）中白细胞计数显著增加（P〈0.01）,α-SMA强阳性表达,气道壁厚度（d/Pi）、气道壁面积（WA/Pi）、气道平滑肌面积（Wam/Pi）和平滑肌细胞计数（N/Pi）均明显增加（P〈0.05或P〈0.01）;与哮喘组对比,APS治疗组和DXM阳性对照组BALF中细胞计数显著减少（P〈0.001）,α-SMA阳性表达,d/Pi、WA/Pi、Wam/Pi和N/Pi均显著减小（P〈0.05或P〈0.01）。结论：APS可抑制哮喘小鼠的气道重塑,这种抑制作用可能是通过调节α-SMA的表达来实现的。

Effects of astragalus polysaccharide on airway remodelling in the asthma modle of mouse

AIM：To evaluate the effects of astragalus polysaccharide（APS） on the airway remodeling in asthmatic mice.METHODS：Sixty SPF BALB/c mouse were randomly divided into four groups：control group,asthmatic model group,APS treatment group and dexamethasone （DXM） treatment group.The experimental groups were sensitized with ovalbumin（OVA）, cured with APS or DXM,then excited with 1% OVA.The method of two-step immunohisto-chemistry and techniques of computer-assisted image analysis were used to detect the changes of the airway remodelling and the expression ofα-SMA. RESULTS：Compared with those in the control group,in asthmatic model group,the counts of inflammation cells were significantly increased（P〈0.01）;the expression ofα-SMA was strongly positive;while the wall thickness （d/Pi） and wall area（WA/Pi） of the bronchi were significantly increased（P〈0.05 or P〈0.01）,and so did the area of smooth muscle （Wam/Pi） and the count of smooth muscle cells （N/Pi）（P〈0.05 or P〈0.01）.Compared with the asthmatic model group,in both APS inhalation group and DXM treatment group,the re- sults ofα-SMA showed positive expression,the numbers of inflammation cells were notably decreased （P〈0.01）,there also were great decreases of d/Pi,WA/Pi,Wam/Pi and N/Pi. CONCLUSION：With the treatment of APS,the course of the airway remodeling can be inhibited. The regulation on the expression level ofα-SMA may be one of the mechanisms controlling the airway remodeling.