TXNIP/NLRP3在脓毒症所致ALI/ARDS患者外周血中的表达

TXNIP/NLRP3expression in peripheral blood of patients with sepsisinduced ALI/ARDS

为探讨硫氧还蛋白互作蛋白(thioredoxin interacting protein,TXNIP)/NOD样受体家族含pyrin结构域蛋白3(NODlike receptor family pyrin domain-containing protein 3,NLRP3)炎症小体通路在急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)发病机制中的作用,收集2017年1月—2018年12月因脓毒症导致急性肺损伤(acute lung injury,ALI)/ARDS重症住院的患者及同期健康体检者各40例为研究对象,其中病例组按照采血时间分为治疗D0、D3、D7组。采用qRT-PCR测定研究对象PBMC中NLRP3和TXNIP mRNA表达水平,同时采用Western blotting测定PBMC中NLRP3和TXNIP的蛋白表达水平。结果显示,病例治疗D0组、D3组、D7组的TXNIP、NLRP3 mRNA和TXNIP、NLRP3蛋白表达水平均显著高于对照组(均P<0.05);病例治疗D7组TXNIP、NLRP3 mRNA表达水平较治疗D0组显著降低(均P<0.05);治疗D3组的TXNIP、NLRP3 mRNA表达水平较治疗D0组显著降低(均P<0.05);病例组TXNIP、NLRP3 mRNA水平均与序贯器官衰竭估计评分(sequential organ failure assessment,SOFA)呈正相关(r≥0.782)。由此,TXNIP/NLRP3炎症小体通路可能参与脓毒症所致ALI/ARDS的发生、发展。

To explore the potential role of thioredoxin interacting protein(TXNIP)and NOD-like receptor family pyrin domaincontaining protein 3(NLRP3)inflammasome in the pathogenesis of acute respiratory distress syndrome(ARDS),40patients with sepsis-induced severe acute lung injury(ALI)/ARDS were selected as the patient group from January 2017to December 2018,and 40individuals who passed health checkup were set as controls.The patient group was subdivided into D0,D3and D7groups according to the treatment duration.The quantitative expressions of NLRP3 and TXNIP mRNA in PBMCs were measured by qRT-PCR,and the expression levels of NLRP3 and TXNIP proteins in PBMCs were detected by Western blotting.The results showed that TXNIP,NLRP3 mRNA and TXNIP,NLRP3protein in patients at D0,D3and D7stages were significantly higher than those in the control group(P<0.05);the levels of TXNIP,NLRP3 mRNA at D7were significantly lower than those at D0(P<0.05);the levels of TXNIP,NLRP3 mRNA at D3were significantly lower than those at D0(P<0.05);the levels of TXNIP,NLRP3 mRNA in the patient group were positively correlated with sequential organ failure assessment(SOFA).In conclusion,TXNIP/NLRP3inflammasome could be involved in the pathogenesis of patients with sepsis-induced severe ALI/ARDS.