目的探讨1-羟基-2,3,5-三甲氧基■酮(QGS)对脂多糖(LPS)致小鼠急性肺损伤的保护作用及其机制。方法采用ipLPS的方法建立小鼠急性肺损伤模型。检测肺脏指数,酶法检测支气管及肺泡灌洗液(BALF)中NO水平,Western blotting法检测核转录因子κB抑制蛋白IκB-α,诱导型一氧化氮合成酶(iNOS)及环氧合酶Ⅱ(COX-2)等蛋白的表达,HE染色观察肺组织病理学改变。结果QGS500mg/kg组能显著降低LPS引起的小鼠的肺脏指数(P<0.05)。QGS250、500mg/kg组均能显著降低LPS致伤小鼠BALF中NO水平,抑制率分别达到了37%和48.1%。同时QGS500mg/kg组还能够明显增加肺组织中IκB-α蛋白表达量并下调iNOS及COX-2蛋白表达量。结论QGS对LPS引起的小鼠急性肺损伤有保护作用,该作用与其增加IκB-α蛋白表达而抑制iN-OS和COX-2蛋白的表达有关。 Objective To investigate the protective effect of 1-hydroxy-2,3,5-trimethoxyxonone (QGS) on acute lung injury induced by lipopolysaccharide (LPS) in mice and its mechanism. Methods The mouse acute lung injury model was established by ipLPS. Lung index was measured, NO levels in bronchial and alveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay, and nuclear factor-κB inhibitory protein IκB-α, inducible nitric oxide synthase (iNOS) and cyclooxygenase II were detected by Western blotting. (COX-2) and other proteins were expressed and HE staining was used to observe the pathological changes of lung tissue. Results The QGS 500mg/kg group significantly reduced the lung index of LPS-induced mice (P<0.05). QGS250, 500mg/kg group can significantly reduce the LPS-induced injury in BALF NO levels, the inhibition rate reached 37% and 48.1%. At the same time, the QGS 500mg/kg group also significantly increased the expression of IκB-α protein in the lung tissue and down-regulated the expression of iNOS and COX-2 protein. Conclusion QGS has a protective effect on LPS-induced acute lung injury in mice. This effect is related to the increase of IκB-α protein expression and inhibition of iN-OS and COX-2 protein expression.