中文摘要：

目的：探究白介素-1β（interleukin-1β,IL-1β）在急性呼吸窘迫综合征（acute respiratory distress syndrome,ARDS）中的表达以及通过自噬调节IL-1β在ARDS中的作用。方法：将小鼠分为脂多糖（lipopolysaccharide,LPS）模型组、LPS＋3-甲基腺嘌呤（3-methyladenine,3-MA）干预组和LPS＋PBS对照组,每组随机分配5只C57BL/6雄性小鼠,通过ELISA检测小鼠血清、肺泡灌洗液中IL-1β的表达,RT-PCR对小鼠肺组织中IL-1β进行定量分析,Western blot检测LPS诱导的ARDS小鼠肺组织中微管相关蛋白LC3（LC3Ⅱ/LC3Ⅰ）以及P62表达,使用3-MA干预ARDS小鼠模型,后检测IL-1β、肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）、白介素-6（interleukin-6,IL-6）、γ-干扰素（interferon-γ,IFN-γ）等细胞因子以及自噬水平变化。结果：1LPS诱导ARDS小鼠模型中,IL-1β在外周血、肺泡灌洗液以及肺组织中的表达较正常对照组明显升高（P值分别为0.000、0.000、0.021）,Western blot检测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处理ARDS小鼠模型后,IL-1β以及TNF-α、IL-6、IFN-γ等细胞因子在外周血、肺泡灌洗液以及肺组织中的表达较对照组和模型组明显降低（P〈0.01）,Western blot检测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）。结论：抑制过度自噬可降低IL-1β水平,减弱IL-1β的促炎作用,调控ARDS的失控性炎症效应。

英文摘要：

Objective：To explore the expression of the interleukin-1β（IL-1β）in severe acute respiratory distress syndrome（ARDS）and the regulation of IL-1βby autophagy in ARDS. Methods：Mice were divided into lipopolysaccharide（LPS）induced ARDS model group,LPS＋3-methyladenine（3-MA）autophagy inhibition intervention group and LPS＋PBS control group;each group were randomly assigned 5 C57BL/6 male mice. The expressions of IL-1βin serum and bronchoalveolar lavage fluid were detected by ELISA. Quantitative analysis of IL-1βin the lung tissue of mice was conducted by RT-PCR. Expressions of LPS induced blot related protein LC3（LC3II/LC3I）and the P62 were detected by Western blot. 3-MA was used to intervene ARDS mouse model,and changes in expressions of tumor necrosis factor-α（TNF-α）,interleukin-6（IL-6）,interferon-γ（IFN-γ）and other cytokines and autophagy levels were detected. Results：1In LPS induced ARDS mice model,the expressions of IL-1βin lung tissue and lavage fluid was obviously higher than those of normal control group in peripheral blood and bronchoalveolar lavage（P=0.000,P=0.000,P=0.021）. P62 protein detected by Western blot（F=14.376,P=0.005）was decreased gradually; the ratio of LC3 was increased gradually（LC3Ⅱ/LC3Ⅰ F=53.799,P=0.000）. 2In 3-MA mouse model of ARDS,IL-1β,TNF-α,IL-6,IFN-γ and cytokine expressions in lung tissue and lavage fluid were significantly lower than those of control group and model group in the peripheral blood and bronchoalveolar lavage（P0.01）. Western blot detection of P62 protein was decreased gradually（F =20.037,P =0.002）,the ratio of LC3 Ⅰ/LC3 Ⅱ was increased gradually（F=38.726,P=0.000）. Conclusion：Inhibiting excessive autophagy can decrease the level of IL-1β and reduce the proinflammatory effect of IL-1β,thus controlling the inflammatory effect of ARDS.