目的：探讨木犀草素（luteolin）对脂多糖（1ipopolysaccharid，LPS）诱导的小鼠急性肺损伤的保护作用，以及可能的作用机制。方法96只小鼠随机分为正常组、模型组、木犀草素低剂量组、木犀草素中剂量组、木犀草素高剂量组及地塞米松组，每组8只。以小鼠气道穿刺滴入LPS制备小鼠ALI模型，呼吸机检测气道吸气阻力（ Ri ）、气道呼气阻力（Re）和动态肺顺应性（Cdyn）的变化，ELISA法测定肺泡灌洗液（BALF）中IL-1β、IL-6和TNF-α的浓度，制作HE病理切片以及Western blot法检测肺组织中NF-κB p65、IκB-α和PIκB-α的表达情况。结果木犀草素能明显抑制Ri、Re增长和Cdyn降低，抑制BALF中IL-1β、IL-6、TNF-α的释放（ P ＜0？．05），减轻了肺部病变，抑制了NF-κB p65和PIκB-α的活化。结论木犀草素对LPS诱导的小鼠急性肺损伤具有保护作用，其作用机制与抑制NF-κB信号传导通路表达有关。%Objective To investigate the effect of luteolin on acute lung injury ( ALI) induced by lipopolysaccharide (LPS) in mice,and to explore possible action mechanism .Methods Ninety-six mice were randomly divided into 6 groups:notmal control group ,model group ,luteolin low-dose group luteolin median-dose group luteolin high-dose group ,dexamethasone control group ,with 8 mice in each group .The animal models with ALI were established by injecting LPS into airway of mice , then the changes of lung airway inspiratory resistance (Ri),expiratory resistance (Re) and dynamic lung compliance (Cdyn) were detected by pulmonary function test apparatus .The levels of IL-1β,IL-6,TNF-αin bronchoalveolar lavage fluid ( BALF) were determined by ELISA .The pathological sections were made ,and the histopathological changes were observed under light microscope.The expression levels of NF-κB p65,IκB-αand PIκB-αin lung tissues were detected by Western blotting .Results Luteolin could obviously inhibit Ri ,Re and reduce Cdyn ,and could significantly decrease the concentrations of IL-1β,IL-6 and TNF-αin BALF ( P <0.05),as a result,which could relieve lung injury ,moreover,luteolin could inhibit the activation of NF-κB p65 and PIκB-α.Conclusion Luteolin has a protective effect on ALI induced by LPS in mice , and its action mechanism is correlated to inhibiting the expression of NF-κB signal transduction pathway .
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