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IL-17A与脂多糖诱导的小鼠急性肺损伤早期反应的关系

郑爽 付秦磊 周玲萍 彭传鹏 徐红蕾

中国临床药理学与治疗学2018,Vol.23Issue(2):148-153,6.
中国临床药理学与治疗学2018,Vol.23Issue(2):148-153,6.DOI:10.12092/j.issn.1009-2501.2018.02.006

IL-17A与脂多糖诱导的小鼠急性肺损伤早期反应的关系

Study on interleukin-17A during early inflammatory response in mice with LPS-induced acute lung injury

郑爽 1付秦磊 1周玲萍 2彭传鹏 3徐红蕾4

作者信息

  • 1. 温州医科大学第一临床医学院,温州325000,浙江
  • 2. 温州医科大学附属第一医院呼吸内科,温州325000,浙江
  • 3. 温州医科大学附属第三医院老年病科,温州325000,浙江
  • 4. 温州医科大学附属第一医院急诊医学科,温州325000,浙江
  • 折叠

摘要

Abstract

AIM:To observe the dynamic changes of IL-17A in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice,and to assess the correlation of IL-17A during early inflammatory response of ALI.METHODS:Mice were used to establish the ALI group and its control group by intratracheal administration of LPS and normal saline,respectively.The level of IL-17A in bronchoalveolar lavage fluid (BALF) and MCP-1 in serum,histopathological changes in lung tissue,lung wet weight/dry weight ratio (W/D),the expression of intercellular adhesion molecule 1 (ICAM-1) and the myeloperoxidase (MPO) activity in lung homogenates would be tested after modeling for 3,8,14,24 h.RESULTS:Compared with the controls,the level of IL-17A in BALF increased (P < 0.05) and the level of MCP-1 in serum increased significantly (P <0.01),and as time went by,the three above decreased gradually,and the histological examination of lung showed inflammatory changes,and W/D ratio,expression of ICAM-1,MPO activity aggravated gradually in the ALI group (P < 0.05).CONCLUSION:The level of IL-17A in BALF increased significantly during early ALI,and this shows that IL-17A may play an important role in the progress of early inflammatory response in LPS-induced ALI.

关键词

急性肺损伤/脂多糖/白介素17A

Key words

acute lung injury/lipopolysaccharide/IL-17A

分类

医药卫生

引用本文复制引用

郑爽,付秦磊,周玲萍,彭传鹏,徐红蕾..IL-17A与脂多糖诱导的小鼠急性肺损伤早期反应的关系[J].中国临床药理学与治疗学,2018,23(2):148-153,6.

基金项目

温州市科技局科研基金(Y20140680) (Y20140680)

浙江省卫生厅科研基金(2015RCB018) (2015RCB018)

浙江省自然科学基金(LY12H01001) (LY12H01001)

中国临床药理学与治疗学

OACSCDCSTPCD

1009-2501

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