Ferulic acid (FA) exhibits anti‐inflammatory, antidiabetic, antihyperlipidemic, antioxidant, neuroprotective, and antihypertensive effects. This study aimed to determine whether FA could ameliorate lipopolysaccharide (LPS)‐induced inflammatory responses and acute lung injury (ALI) in mice. Mice were challenged with LPS intratracheally to induce ALI 1 h after 3 days of FA (25, 50, and 100 mg/kg) or dexamethasone (DEX; 5 mg/kg) administration. The lung tissues and bronchoalveolar lavage fluid (BALF) were collected 12 h after the LPS challenge. Pretreatment with FA or DEX could attenuate lung histopathological change, complement deposition, and lung wet‐to‐dry weight ratio of mice injured by LPS. Meanwhile, the influx of neutrophils and macrophages, as well as the production of proinflammatory cytokine (tumor necrosis factor‐alpha, interleukin 1 beta [IL‐1β], and IL‐6), in BALF of ALI mice was significantly decreased. Moreover, FA or DEX markedly reversed the LPS‐induced elevation of myeloperoxidase activity and monocyte chemoattractant protein‐1 level in lung tissues of ALI mice. In addition, the Western blot analysis demonstrated that FA or DEX effectively inhibited the LPS‐induced activation of the toll‐like receptor 4 (TLR4)/nuclear factor‐kappa B (NF‐κB) signaling pathway in lung tissues. The current study suggested that the alleviating effect of FA against LPS‐induced ALI might be partially due to the inhibition of the inflammatory response via inactivation of the TLR4/NF‐κB signaling pathway.

中文翻译：

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阿魏酸通过抑制TLR4 /NF-κB信号通路减轻脂多糖诱导的急性肺损伤

阿魏酸（FA）表现出抗炎，抗糖尿病，抗高血脂，抗氧化剂，神经保护和降压作用。这项研究旨在确定FA是否可以改善脂多糖（LPS）诱导的小鼠炎症反应和急性肺损伤（ALI）。给予FA（25、50和100 mg / kg）或地塞米松（DEX; 5 mg / kg）3天后，气管内LPS激发小鼠诱导ALI。LPS攻击后12小时收集肺组织和支气管肺泡灌洗液（BALF）。用FA或DEX预处理可以减轻LPS损伤的小鼠的肺组织病理学变化，补体沉积和肺干重比。同时，中性粒细胞和巨噬细胞的大量涌入，以及促炎性细胞因子（肿瘤坏死因子-α，ALI小鼠的BALF中的白介素1β[IL-1β]和IL-6）显着降低。此外，FA或DEX可以明显逆转LP诱导的ALI小鼠肺组织中髓过氧化物酶活性和单核细胞趋化蛋白1的升高。此外，蛋白质印迹分析表明FA或DEX可有效抑制LPS诱导的肺组织中Toll样受体4（TLR4）/核因子κB（NF-κB）信号通路的激活。目前的研究表明，FA对LPS诱导的ALI的缓解作用可能部分归因于通过TLR4 /NF-κB信号通路失活抑制了炎症反应。FA或DEX可以明显逆转LP诱导的ALI小鼠肺组织中的髓过氧化物酶活性和单核细胞趋化蛋白1的升高。此外，蛋白质印迹分析表明FA或DEX可有效抑制LPS诱导的肺组织中Toll样受体4（TLR4）/核因子κB（NF-κB）信号通路的激活。当前的研究表明，FA对LPS诱导的ALI的缓解作用可能部分归因于通过TLR4 /NF-κB信号通路失活抑制了炎症反应。FA或DEX可以明显逆转LP诱导的ALI小鼠肺组织中的髓过氧化物酶活性和单核细胞趋化蛋白1的升高。此外，蛋白质印迹分析表明FA或DEX可有效抑制LPS诱导的肺组织中Toll样受体4（TLR4）/核因子κB（NF-κB）信号通路的激活。目前的研究表明，FA对LPS诱导的ALI的缓解作用可能部分归因于通过TLR4 /NF-κB信号通路失活抑制了炎症反应。