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作 者:姜江 荣光[1] 谢展利 高晨慧 倪凯茹[1] 石怡珍[1] JIANG Jiang;RONG Guang;XIE Zhanli;GAO Chenhui;NI Kairu;SHI Yizhen(Department of Nuclear Medicine,the Second Affiliated Hospital of Soochow University,Suzhou 215004;Jiangsu Institute of Hematology,the First Affiliated Hospital of Soochow University)
机构地区:[1]苏州大学附属第二医院核医学科,苏州215004 [2]苏州大学附属第一医院江苏省血液研究所
出 处:《南通大学学报(医学版)》2019年第2期81-84,共4页Journal of Nantong University(Medical sciences)
基 金:国家自然科学基金青年基金资助项目(81800128)
摘 要:目的:研究肺泡上皮细胞的平足蛋白(podoplanin, PDPN)在急性肺损伤中的作用。方法:将内毒素(lipopolysaccharide, LPS)经气管内滴注于小鼠肺部造成急性肺损伤,观察并比较野生型小鼠和上皮细胞PDPN敲除小鼠肺组织的病理变化及肺泡灌洗液中的炎性指标。结果:野生型小鼠在滴注LPS 6 h 后,肺泡上皮细胞PDPN含量明显增高,说明LPS 在体内可诱导PDPN的表达。在LPS 滴注24 h 后,PDPN 敲除小鼠的肺组织炎症反应明显,肺微血管充血扩张,肺间质增生严重,肺间质和肺泡内有大量炎症细胞浸润,而野生型小鼠则无明显病理变化。与野生型小鼠相比,PDPN敲除小鼠支气管肺泡灌洗液中的蛋白含量及总细胞数明显升高,肺组织髓过氧化物酶活性也显著增高。提示肺泡上皮细胞PDPN基因的缺陷加剧内毒素所致的急性肺损伤。结论:肺泡上皮细胞PDPN在内毒素介导的急性肺损伤中具有重要的调控作用。Objective : To study the role of podoplanin(PDPN) in alveolar epithelial cell in acute lung injury. Methods: By tracheal instillation of lipopolysaccharide(LPS) into wild-type(WT) and PDPN-deficient m ice, w e o bserved t he l ung pathological changes and inflammatory makers of bronchoalveolar lavage fluid. Results : Compared with that at the beginning, PDPN level in WT mice was obviously increased at 6 hours after LPS injection. 24 hours after LPS injection, the HE staining indicated that the lung of PDPN-deficient mice exhibited significantly enhanced inflammation, interstitial proliferation, leukocyte infiltration and vasodilator. However, the lung of WT m ice e xperienced m inor c hanges. Moreover, compared with WT mice, the total cell numbers and protein concentration in the BAL fluid from PDPN-deficient mice increased significantly 24 hours after LPS injection. Besides, myeloperoxidase activity in PDPN-deficient lung was significantly enhanced compared with that of WT lung. Conclusion : PDPN is a key mediator in the inflammatory response to acute lung injury.
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