本文選題：白介素-β + 急性呼吸窘迫綜合征�。� 參考：《重慶醫(yī)科大學學報》2017年01期

【摘要】：目的:探究白介素-1β(interleukin-1β,IL-1β)在急性呼吸窘迫綜合征(acute respiratory distress syndrome,ARDS)中的表達以及通過自噬調(diào)節(jié)IL-1β在ARDS中的作用。方法:將小鼠分為脂多糖(lipopolysaccharide,LPS)模型組、LPS+3-甲基腺嘌呤(3-methyladenine,3-MA)干預組和LPS+PBS對照組,每組隨機分配5只C57BL/6雄性小鼠,通過ELISA檢測小鼠血清、肺泡灌洗液中IL-1β的表達,RT-PCR對小鼠肺組織中IL-1β進行定量分析,Western blot檢測LPS誘導的ARDS小鼠肺組織中微管相關(guān)蛋白LC3(LC3Ⅱ/LC3Ⅰ)以及P62表達,使用3-MA干預ARDS小鼠模型,后檢測IL-1β、腫瘤壞死因子-α(tumor necrosis factor-α,TNF-α)、白介素-6(interleukin-6,IL-6)、γ-干擾素(interferon-γ,IFN-γ)等細胞因子以及自噬水平變化。結(jié)果:1LPS誘導ARDS小鼠模型中,IL-1β在外周血、肺泡灌洗液以及肺組織中的表達較正常對照組明顯升高(P值分別為0.000、0.000、0.021),Western blot檢測P62蛋白逐步降低(F=14.376,P=0.005),LC3Ⅱ/LC3Ⅰ值逐步升高(F=53.799,P=0.000);23-MA處理ARDS小鼠模型后,IL-1β以及TNF-α、IL-6、IFN-γ等細胞因子在外周血、肺泡灌洗液以及肺組織中的表達較對照組和模型組明顯降低(P0.01),Western blot檢測P62蛋白逐步降低(F=20.037,P=0.002),LC3Ⅰ/LC3Ⅱ值逐步升高(F=38.726,P=0.000)。結(jié)論:抑制過度自噬可降低IL-1β水平,減弱IL-1β的促炎作用,調(diào)控ARDS的失控性炎癥效應(yīng)。
[Abstract]:Aim: to investigate the expression of interleukin-1 尾 (IL-1 尾) in acute respiratory distress syndrome (ARDS) and the role of IL-1 尾 in ARDS by autophagy. Methods: the mice were divided into LPS-3-methyladenine 3-MA-intervention group and LPS PBS control group. Five C57BL/6 male mice were randomly assigned to each group. The serum of the mice was detected by ELISA. Expression of IL-1 尾 in alveolar lavage fluid and quantitative analysis of IL-1 尾 in mouse lung tissue by RT-PCR the expression of microtubule associated protein LC3(LC3 鈪，

本文編號：1835618