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[1]张敏龙,金发光.MiR-138-5p通过抑制SIRT1表达增强了海水吸入性肺损伤中炎症反应[J].中华肺部疾病杂志,2023,(06):751-755.[doi:10.3877/cma.j.issn.1674-6902.2023.06.001]
 Zhang Minlong,Jin Faguang..MiR-138-5p enhanced the inflammation in seawater aspiration-induced acute lung injury via inhibition the expression of SIRT1[J].,2023,(06):751-755.[doi:10.3877/cma.j.issn.1674-6902.2023.06.001]
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MiR-138-5p通过抑制SIRT1表达增强了海水吸入性肺损伤中炎症反应(PDF)

《中华肺部疾病杂志》[ISSN:1006-6977/CN:61-1281/TN]

卷:
期数:
2023年06期
页码:
751-755
栏目:
论著
出版日期:
2023-12-20

文章信息/Info

Title:
MiR-138-5p enhanced the inflammation in seawater aspiration-induced acute lung injury via inhibition the expression of SIRT1
作者:
张敏龙12金发光2
100091 北京,解放军总医院第八医学中心呼吸与危重症医学部1
710038 西安,空军军医大学唐都医院呼吸科2
Author(s):
Zhang Minlong12 Jin Faguang1.
1Department of Respiratory and Critical Care Medicine, the Eighth Medical Center, PLA General Hospital, Beijing 100091, China; 2Department of Respiratory, Tangdu Hospital, Air Force Military Medical University, Xi'an 710032, China
关键词:
急性肺损伤 海水 SIRT1通路 miR-138-5p
Keywords:
Acute lung injury Seawater SIRT1 pathway miR-138-5p
分类号:
R563
DOI:
10.3877/cma.j.issn.1674-6902.2023.06.001
摘要:
目的 观察miR-138-5p在海水吸入性肺损伤(acute lung injury, ALI)中的作用及机制。 方法 分别构建海水吸入性肺损伤大鼠及大鼠肺血管内皮细胞(rat pulmonary vascular endothelial cells, RPMVECs)细胞模型,分为空白对照组、海水处理组、miR-138-5p antagomir预处理组和antag NC预处理组。观察肺组织湿干比、伊文思蓝法检测肺微血管通透性,用ELISA法检测肺组织及细胞中肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)、白介素-1β(interleukin-1β, IL-1β)和白介素-6(interleukin-6, IL-6)的含量,western blot检测SIRT1及乙酰化(Acetyl)-核因子-κB(nuclear factor kappa-B, NF-κB)的表达变化,采用双荧光素酶报告基因实验验证SIRT1和miR-138-5p的作用关系。 结果 海水干预4 h后,大鼠肺组织湿干比及通透性明显增加,组织及细胞中TNF-α、IL-1β和IL-6的含量增高,miR-138-5p表达明显增高,SIRT1表达出现了下降,Acetyl-NF-κB的表达明显升高。而抑制miR-138-5p的表达后,炎症反应得到了明显的减轻,SIRT表达出现了回升,Acetyl-NF-κB的表达出现了下降。 结论 增加表达的miR-138-5p在海水吸入性肺损伤炎症的发展中起到了关键作用,这种作用是通过调节SIRT1通路形成的。
Abstract:
Objective To observe the role and mechanism of miR-138-5p in seawater aspiration-induced acute lung injury(ALI). Methods Rats and rat pulmonary vascular endothelial cells(RPMVECs)seawater aspiration induced ALI models were established and were divided into 4 groups: normal control group, seawater group, miR-138-5p antagomir group and antag NC pre-treated group. W/D ratio and Evans blue were carried out after modeling. The contents of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β)and interleukin-6(IL-6)were measured by enzyme linked immunosorbent serologic assay(ELISA)and the expression of SIRT1 and Acetyl-nuclear factor kappa-B(NF-κB)were measured by western blot. Doubleluciferase reporter gene assay was used to verify the functional relationship between SIRT1 and miR-138-5p. Results After 4 h seawater stimulation, W/D ratio and Evans blue were obvious and the contents of TNF-α, IL-1β and IL-6 were increased. The expression of miR-138-5p, Acetyl-NF-κB were increased and SIRT1 expression was inhibited. Inhibition of miR-138-5p decreased the inflammation, oxidative stress and Acetyl-NF-κB and increased the expression of SIRT1. Conclusion These results suggest that increased expression of miR-138-5p was an important cause in seawater-induced ALI and this phenomenon was through SIRT1 pathway.

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备注/Memo

备注/Memo:
基金项目: 解放军总医院第八医学中心国科金配套基金(QN202211004)
通信作者: 金发光, Email: jinfag@fmmu.edu.cn
更新日期/Last Update: 2023-12-20