中国临床解剖学杂志 ›› 2016, Vol. 34 ›› Issue (5): 523-527.doi: 10.13418/j.issn.1001-165x.2016.05.010

• 实验研究 • 上一篇    下一篇

地塞米松对急性肺损伤中TREM-1表达的影响

骆凤1, 郑浩翔2, 董良3, 李年旺2, 周琴2, 贾哲2, 贺丽萍1, 孙国瑛1,4   

  1. 1.湖南师范大学医学院基础医学系组织学与胚胎学教研室,  长沙   410013;    2. 湖南师范大学树达学院
    2014级临床医学专业,  长沙   410013;    3. 遵义医学院附属医院麻醉科,  遵义   563000;   
    4.中南大学基础医学院,  长沙   410006
  • 收稿日期:2016-04-21 出版日期:2016-09-25 发布日期:2016-10-14
  • 通讯作者: 孙国瑛,博士,硕士生导师,E-mail:sunguoying1029@ 163.com
  • 作者简介:骆凤(1992-),女,湖南岳阳人,学士,在读硕士,主要研究方向:呼吸系统疾病损伤与修复机制研究,Tel:0731-88912441,E-mail:13973161724@163.com
  • 基金资助:

    湖南省教育厅科研项目(14C0703);中南大学博士后基金(160320001);2015年湖南师范大学树达学院创新课题(012-615)

Effect of dexamethasone on the expression of TREM-1 in acute lung injury

LUO Feng1, ZHENG Hao-xiang2, DONG Liang3, LI Nian-wang2, ZHOU Qin2, JIA Zhe2, HE Li-ping 1, SUN Guo-ying 1,4   

  1. 1.Department of Histology and Embryology, Hunan Normal University, Changsha 410013; 2. Clinical Medical Undergraduates of Grade 2014, College of Shu Da, Hunan Normal University, Changsha 410013; 3.Department of Anesthesiology, Affiliated Hospital of Zunyi Medical College, Zunyi 563000;4. College of Basic Medical Sciences, Central South University, Changsha 410006, China
  • Received:2016-04-21 Online:2016-09-25 Published:2016-10-14

摘要:

目的 探讨地塞米松(Dexamethasone,Dex)对脂多糖(Lipopolysaccharide, LPS)诱导的急性肺损伤(acute lung injury, ALI)小鼠肺组织中髓样细胞表达的触发受体1(triggering receptor expressed on myeloid cells-1,TREM-1)表达的影响。 方法 以昆明小鼠为研究对象,腹腔注射LPS(10 mg/kg)建立ALI模型,30 min后给予不同浓度的Dex(5、10、20、40 mg/kg)处理6 h;选用Dex(10 mg/kg)处理不同的时间(6、12、24、36 h)。HE染色法观察肺组织病理损伤程度; RT-PCR检测肺组织TREM-1mRNA的表达;ELISA检测小鼠支气管肺泡灌洗液中可溶性TREM-1(sTREM-1)蛋白水平。  结果 Dex可减轻肺病理损伤;Dex呈时间依赖性地下调ALI小鼠肺组织的TREM-1 mRNA的表达,且在6 h即可降低;Dex呈剂量依赖地下调ALI小鼠肺组织中TREM-1 mRNA的表达,并在10 mg/kg时开始降低。Dex可降低ALI小鼠支气管肺泡灌洗液中sTREM-1的蛋白水平。  结论 Dex可呈剂量及时间依赖性下调ALI小鼠肺组织中的TREM-1mRNA的表达,并减少肺内髓样细胞胞膜TREM-1的脱落,提示Dex可能通过调节TREM-1的表达,从而抑制ALI早期的炎症级联反应,参与保护肺组织。

关键词: 髓样细胞表达的触发受体-1, 急性肺损伤, 地塞米松, 脂多糖

Abstract:

Objective To investigate the effects of dexamethasone (Dex) on the TREM-1expression in acute lung injury(ALI) of mice induced by lipopolysaccharide (LPS). Methods  Kunming mice (KM mice) were used as the research object and LPS (10 mg/kg) was used to induce acute lung injury model. After half an hour given different concentrations of Dex (5, 10, 20, 40 mg/kg) and selection of different time points (6, 12, 24 and 36 h) were observed. The lung tissue was observed by HE staining, RT-PCR was used to detect TREM-1 expression, and ELISA was used to detect the expression of sTREM-1 in bronchoalveolar lavage fluid of mice.    Results    Dex could time-dependently down-regulate the expression of lung tissue in the acute lung injury and in 6h treatment peak; Dexcould dose-dependently down-regulate TREM-1 expression in acute lung injury of lung tissue, and reached the peak at 10 mg /kg. Dex could decrease the protein level of sTREM-1 in bronchoalveolar lavage fluid of ALI mice. Conclusion Dex can down-regulate TREM-1 of lung tissues of ALI mice in a dose and time-dependent manner, and reduce myeloid cell membrane of TREM-1 in lung. Our research indicates that Dex may inhibit inflammatory cascade and protect lung tissue by regulation of TREM-1 expression.

Key words: Triggering receptor expressed on myeloid cells-1, Acute lung injury, Dexamethasone;Lipopolysaccharide