【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。更多还原

【Abstract】 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-1β in 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.更多还原