CTRP3通过SIRT1/NF-κB信号通路改善脂多糖诱导的小鼠急性肺损伤  

CTRP3 ameliorates lipopolysaccharides-induced acute lung injury in mice through SIRT1/NF-κB signaling pathway

作　　者：刘芳 王布[1] 张长洪[2] 邹芳 郭志青 宋宇烜 刘建华[2] LIU Fang;WANG Bu;ZHANG Changhong;ZOU Fang;GUO Zhiqing;SONG Yuxuan;LIU Jianhua(Department of Respiratory and Critical Care Medicine,The First Affiliated Hospital of Hebei North University,Zhangjiakou 075000,Hebei,China;RICU,The First Affiliated Hospital of Hebei North University,Zhangjiakou 075000,Hebei,China)

机构地区：[1]河北北方学院附属第一医院呼吸与危重症医学科,河北张家口075000 [2]河北北方学院附属第一医院RICU,河北张家口075000

出　　处：《西部医学》2023年第1期28-33,共6页Medical Journal of West China

基　　金：河北省2021年度医学科学研究项目(0210267)。

摘　　要：目的探究CTRP3对脂多糖(LPS)诱导的急性肺损伤(ALI)的保护性机制。方法在小鼠气管内滴注3 mg/kg LPS建立ALI模型,并随机分为对照组、LPS组、LPS+LV-NC和LPS+LV-CTRP3组4组。采用定量实时聚合酶链反应法(qRT-PCR)检测肺组织中CTRP3的表达水平;HE染色用于评估肺组织学;采用酶联免疫吸附试验(ELISA)检测支气管肺泡灌洗液(BALF)中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6和白细胞介素-1β的表达;试剂盒检测SOD,CAT,GSH-Px和MDA含量变化;Western blot检测机制相关蛋白的表达。结果与对照组比较,ALI小鼠肺组织中CTRP3的表达显著降低(P<0.05)。与LPS组比较,CTRP3过表达可减轻病理损伤;显著减少总炎症细胞和中性粒细胞计数(P<0.05);抑制炎症介质释放和氧化应激反应(P<0.05);激活沉默信息调节器1(SIRT1)调节p65磷酸化和p53乙酰化(P<0.05)。结论CTRP3通过调节SIRT1介导的NF-κB/p53信号通路在ALI小鼠中发挥保护作用,这是一种有希望的ALI治疗策略。Objective To explore the protective mechanism of CTRP3 on lipopolysaccharide(LPS)-induced acute lung injury(ALI).Methods ALI model was established by injecting 3 mg/kg LPS into the trachea of mice,and the mice were randomly divided into 4 groups:control group,LPS group,LPS+LV-NC group and LPS+LV-CTRP3 group.The expression level of CTRP3 in lung tissues was detected by quantitative real-time polymerase chain reaction(qRT-PCR).HE staining was used to evaluate lung histology.The expressions of tumor necrosis factor(TNF)-α,interleukin(IL)-6 and IL-1βin bronchoalveolar lavage fluid(BALF)were determined by enzyma-linked immunosorbent assay(ELISA).The contents of SOD,CAT,GSH-Px and MDA were detected by the kit.Western blot was used to detect the expression of mechanism-related proteins.Results Compared with the control group,the expression of CTRP3 in ALI mice lung tissue was significantly decreased(P<0.05).Compared with LPS group,overexpression of CTRP3 could alleviate pathological injury,significantly reduce the total inflammatory cells and neutrophils(P<0.05),inhibit the release of inflammatory mediators and oxidative stress response(P<0.05).Overexpression of CTRP3 activated silencing information modulator 1(SIRT1)to regulate p65 phosphorylation and p53 acetylation(P<0.05).Conclusion CTRP3 plays a protective role in ALI mice by regulating NF-κB/p53 signaling pathway mediated by SIRT1,which is a promising treatment strategy for ALI.

关 键 词：CTRP3 肺损伤 炎症反应 氧化应激 

分 类 号：R563[医药卫生—呼吸系统]