目的：研究NS1619在哮喘小鼠气道重塑中的作用。方法 BALB/c雌性小鼠24只，随机分为对照组、卵清蛋白OVA致敏/激发组(哮喘组)和NS1619干预组(干预组)，每组8只。以卵清蛋白致敏，第19天予5% OVA连续吸入激发5 d后，改为3次/周，直至第55天，建立哮喘小鼠气道重塑模型。干预组于每次OVA吸入激发前2 h先吸入30μmol/L NS1619雾化液20 min。对照组以等量生理盐水腹腔注射和雾化代替。光镜下观察HE染色、Masson染色的肺组织切片， Image-pro plus图像处理软件定量分析平滑肌厚度和胶原沉积，免疫组化法观察并测定气道平滑肌肌动蛋白(α-SMA)水平，酶联免疫吸附法测定小鼠血清血小板衍生生长因子-BB(PDGF-BB)水平。结果与哮喘组相比，干预组小鼠的肺组织病理学改变并不明显，其平滑肌厚度、胶原沉积面积、α-SMA和PDGF-BB水平均低于哮喘组，差异有统计学意义(P<0.05)。结论 NS1619部分抑制哮喘小鼠气道重塑的形成，可能部分与NS1619下调α-SMA及PDGF-BB表达有关。%Objective To study the mechanism of NS1619 on airway remodeling in asthmatic mice. Methods A total of 24 healthy female BALB/c mice were randomly divided into 3 groups:the control group, the oval albumin (OVA) group (the asthma group) and the NS1619 group (the intervention group), 8 mice in each group. Asthma group was induced with OVA, chal-lenged by continuous inhalation with 5%OVA from day 19 to 23, then changed to 3 times per week from day 24 to 55. Interven-tion group was inhaled with NS1619 (30μmol/L) before OVA. Control group was given with normal saline. The thickness of air-way smooth muscle and the area of collagen deposition in lung tissue slices were observed by HE and Masson staining, measured by a computer assisted image analysis system. The concentration ofα-smooth muscle actin (α-SMA) in cells was detected by immunohistochemistry. The expression of platelet derived grouth factor-BB, PDGF-BB (PDGF-BB) in serum was measured by immunosorbent assay. Results Compared with the asthma group, the pathologic changes of lung tissue, the thickness of airway smooth muscle and collagen deposition in the group treated with NS1619 were signiifcantly decreased (P<0.05). Compared with the asthma group, the levels ofα-SMA in cells and PDGF-BB in serum in NS1619 treated group were signiifcantly decreased (P<0.05). Conclusions NS1619 partly inhibited airway remodeling in asthmatic mice, partially by down-regulating the expres-sion level ofα-SMA and PDGF-BB.
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