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Ferulic acid alleviates lipopolysaccharide‐induced acute lung injury through inhibiting TLR4/NF‐κB signaling pathway
Author(s) -
Wu Xialei,
Lin Liyao,
Wu Haibin
Publication year - 2021
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22664
Subject(s) - bronchoalveolar lavage , tlr4 , pharmacology , proinflammatory cytokine , chemistry , lipopolysaccharide , tumor necrosis factor alpha , alveolar macrophage , western blot , nf κb , lung , inflammation , signal transduction , immunology , endocrinology , medicine , macrophage , biochemistry , in vitro , gene
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.