title: Arctigenin attenuates lipopolysaccharide-induced acute lung injury in rats.
abstract: Arctigenin (ATG) has been reported to possess anti-inflammatory properties. However, the effects of ATG on lipopolysaccharide (LPS)-induced acute lung injury (ALI) remains not well understood. In the present study, our investigation was designed to reveal the effect of ATG on LPS-induced ALI in rats. We found that ATG pretreatment attenuated the LPS-induced ALI, as evidenced by the reduced histological scores, myeloperoxidase activity, and wet-to-dry weight ratio in the lung tissues. This was accompanied by the decreased levels of tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-1 (IL-6) in the bronchoalveolar lavage fluid. Furthermore, ATG downregulated the expression of nuclear factor kappa B (NF-κB) p65, promoted the phosphorylation of inhibitor of nuclear factor-κB-α (IκBα) and activated the adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPKα) in the lung tissues. Our results suggested that ATG attenuates the LPS-induced ALI via activation of AMPK and suppression of NF-κB signaling pathway.
authors.affiliation: Department of Pharmacy, First Affiliated Hospital of Liaoning Medical University, Jinzhou, 121001, Liaoning Province, People's Republic of China.
authors.forename: Xianbao
authors.initials: X
authors.lastname: Shi
authors.forename: Hongzhi
authors.initials: H
authors.lastname: Sun
authors.forename: Dun
authors.initials: D
authors.lastname: Zhou
authors.forename: Huanjiu
authors.initials: H
authors.lastname: Xi
authors.forename: Lina
authors.initials: L
authors.lastname: Shan
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D055371:Acute Lung Injury / Q000188:drug therapy*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D015536:Down-Regulation; D004789:Enzyme Activation / Q000187:drug effects; D005663:Furans / Q000627:therapeutic use*; D020672:I-kappa B Proteins / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D017705:Lignans / Q000627:therapeutic use*; D008070:Lipopolysaccharides; D008168:Lung / Q000473:pathology; D008297:Male; D000072000:NF-KappaB Inhibitor alpha; D020556:Neutrophil Infiltration / Q000187:drug effects / Q000276:immunology; D009195:Peroxidase / Q000378:metabolism; D010766:Phosphorylation; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D051996:Transcription Factor RelA / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D005663:Furans; D020672:I-kappa B Proteins; C000594089:IL1B protein, rat; D053583:Interleukin-1beta; D015850:Interleukin-6; D017705:Lignans; D008070:Lipopolysaccharides; C000606206:Nfkbia protein, rat; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D000072000:NF-KappaB Inhibitor alpha; D009195:Peroxidase; D055372:AMP-Activated Protein Kinases; C568305:Prkaa1 protein, rat; C071942:arctigenin