%0 Journal Article %T 黄芪多糖APS- Ⅱ- 2对脂多糖所致绒毛膜羊膜炎诱发的肺泡化阻滞的改善作用<br>Effect of APS-Ⅱ-2 on intra-amniotic lipopolysaccharide-induced alveolarization arrest in bronchopulmonary dysplasia model rats %A 李文 %A 谈珍 %A 刘成博 %A 王铮涛 %A 张拥军 < %A br> %A LI Wen %A TAN Zhen %A LIU Cheng-bo %A WANG Zheng-tao %A ZHANG Yong-jun %J 上海交通大学学报（医学版） %D 2018 %R 10.3969/j.issn.1674-8115.2018.04.004 %X 目的·探讨黄芪多糖APS-Ⅱ-2对脂多糖（lipopolysaccharide，LPS）所致绒毛膜羊膜炎诱发的肺泡化阻滞的改善作用及可能机制。方法·对孕16.5 d SD大鼠羊膜腔注射LPS，构建支气管肺发育不良模型。根据羊膜腔注入药物，将孕鼠随机分为对照组（Saline组）、LPS+Saline组、LPS+APS-Ⅱ-2组。LPS+APS-Ⅱ-2组新生鼠出生后第1～3日腹腔注射APS-Ⅱ-2溶液[50 mg/（kg·d）]；Saline组和LPS+Saline组腹腔注射等体积生理盐水。取第1、3日新生鼠肺组织，苏木精-伊红（H-E）染色观察病理改变。SD大鼠骨髓巨噬细胞培养，分为PBS组、LPS+PBS组、LPS+APS-Ⅱ-2组，利用全转录组测序技术（RNA-sequence）筛选APS-Ⅱ-2抑制炎症的可能靶点。结果· APS-Ⅱ-2可改善新生鼠肺组织病理状态，LPS+APS-Ⅱ-2组大鼠出生第1日肺泡数较LPS+Saline组增多（P0.033），第1、3日次级突起增多（P0.002，P0.026），第1、3日平均内衬间隔减小（P0.006，P0.004）。RNA-sequence结果显示APS-Ⅱ-2抑制一些炎症因子表达，如Toll样受体Tlr3、Tlr7、Tlr8；也促进一些有抗炎作用因子的表达，如花生四烯酸15-脂加氧酶Alox15和CD74。结论· APS-Ⅱ-2可通过调节炎症反应减轻LPS诱发的绒毛膜羊膜炎，进而改善支气管肺发育不良模型肺组织病理状态。<br>：Objective · To investigate the role of APS-Ⅱ-2 (a kind of plant-derived natural drug) on amelioration of chorioamnionitis-induced alveolarization arrest and the underlying mechanism. Methods · Bronchopulmonary dysplasia (BPD) model was constructedintra-amniotic injection of lipopolysaccharide(LPS) in SD rats (E16.5). The SD rats were randomly divided into control group (Saline group)、LPS model group (LPS+Saline group) and APS-Ⅱ-2administration group (LPS+APS-Ⅱ-2 group). Then neonatal rats in LPS+APS-Ⅱ-2 group were given an intraperitoneal injection with APS-Ⅱ-2 (50 mg/kg) for 3 consecutive days after birth, whereas rats in LPS+Saline group and Saline group were administrated with an equal amount of normal saline. To examine pathologic change of pulmonary in neonatal rats, hematoxylin-eosin (H-E) staining was performed at postnatal day1 and 3. Then bone marrow-derived macrophages (BMDMs) SD rats were detectedthe technology of RNA-sequence to research the immunomodulation of APS-Ⅱ-2.Results · APS-Ⅱ-2 administration group had drastically higher terminal air spaces (P0.033 at postnatal day1) and secondary septa counts at postnatalday1 and 3, respectively (P0.002, P0.026) than LPS-induced model group, while mean linear intercept was the opposite situation at postnatal day1and 3, respectively (P0.006, P0.004). The detection of RNA-sequence indicated that APS-Ⅱ-2 suppressed the of inflammatory cytokines such as Tlr3, Tlr7 and Tlr8 in BMDMs. Meanwhile, it also promoted some pleiotropic cytokines with anti-inflammatory effects such as Alox15 and Cd74. Conclusion · Administration of APS-Ⅱ-2 could improve the pathology of BPD, thereby supporting the ethno pharmacological uses of the plant. This effect may be directly causedmodulatory effects of APS-Ⅱ-2 on inflammation %K 支气管肺发育不良 %K 黄芪多糖 %K 绒毛膜羊膜炎 %K 炎症 %K < %K br> %K bronchopulmonary dysplasia %K APS-Ⅱ-2 %K chorioamnionitis %K inflammation %U http://xuebao.shsmu.edu.cn/CN/abstract/abstract11885.shtml