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(P<0.01). 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.