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首页> 外文期刊>Journal of biochemical and molecular toxicology >Ferulic acid alleviates lipopolysaccharide-induced acute lung injury through inhibiting TLR4/NF-kappaB signaling pathway
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Ferulic acid alleviates lipopolysaccharide-induced acute lung injury through inhibiting TLR4/NF-kappaB signaling pathway

机译：阿魏酸可通过抑制TLR4 / NF-κB信号通路来减轻脂多糖诱导的急性肺损伤

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摘要

Ferulic acid (FA) exhibits anti-inflammatory, antidiabetic, antihyperlipidemic, anti-oxidant, 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 bronch-oalveolar lavage fluid (BALF) were collected 12 h after the LPS challenge. Pre-treatment 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-1beta], 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-kappaB) 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-kappaB signaling pathway.
机译：阿魏酸（FA）具有抗炎、降糖、降血脂、抗氧化、神经保护和降压作用。本研究旨在确定FA是否能改善脂多糖（LPS）诱导的小鼠炎症反应和急性肺损伤（ALI）。在给予FA（25、50和100 mg/kg）或地塞米松（DEX；5 mg/kg）3天后，用LPS气管内激发小鼠以诱导ALI。在LPS激发后12小时收集肺组织和支气管肺泡灌洗液（BALF）。FA或DEX预处理可减轻LPS损伤小鼠的肺组织病理学改变、补体沉积和肺湿干重比。同时，ALI小鼠BALF中中性粒细胞和巨噬细胞的流入以及促炎细胞因子（肿瘤坏死因子α、白细胞介素1β[IL-1β]和IL-6）的产生显著减少。此外，FA或DEX可显著逆转LPS诱导的ALI小鼠肺组织髓过氧化物酶活性和单核细胞趋化蛋白-1水平的升高。此外，Western blot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是由于通过激活TLR4/NF-κB信号通路抑制炎症反应。

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