title: Punicalagin ameliorates lipopolysaccharide-induced acute respiratory distress syndrome in mice.
abstract: Punicalagin, a bioactive ellagitannin isolated from pomegranate, has been reported to have anti-inflammatory property. In the present study, we analyzed the role of punicalagin against acute respiratory distress syndrome (ARDS) induced by lipopolysaccharide (LPS) in mice. Male BALB/c mice with ARDS, induced by intranasal instillation of LPS, were treated with punicalagin 1 h prior to LPS exposure. The effects of punicalagin on pro-inflammatory cytokines, myeloperoxidase activity, nuclear factor kappa B (NF-κB) activation, and the histopathological changes were evaluated. The results showed that punicalagin treatment attenuated LPS-induced lung edema, elevating TNF-α, IL-6, and IL-1β levels in the bronchoalveolar lavage fluid (BALF). Meanwhile, punicalagin significantly inhibited LPS-induced increases in the macrophage and neutrophil infiltration of lung tissues and myeloperoxidase activity. Furthermore, punicalagin inhibits Toll-like receptor 4 (TLR4) expression and NF-κB activation induced by LPS. In conclusion, this is the first study to demonstrate that punicalagin protects against LPS-induced ARDS in mice. The underlying mechanisms may include inhibition of TLR4-mediated NF-κB signaling pathways.
authors.affiliation: Department of Oncology, The General Hospital of Chengdu Military District, Chengdu, Sichuan, 610000, People's Republic of China.
authors.forename: Jingjing
authors.initials: J
authors.lastname: Peng
authors.forename: Dong
authors.initials: D
authors.lastname: Wei
authors.forename: Zengqiang
authors.initials: Z
authors.lastname: Fu
authors.forename: Dong
authors.initials: D
authors.lastname: Li
authors.forename: Yong
authors.initials: Y
authors.lastname: Tan
authors.forename: Tao
authors.initials: T
authors.lastname: Xu
authors.forename: Jinjun
authors.initials: J
authors.lastname: Zhou
authors.forename: Tao
authors.initials: T
authors.lastname: Zhang
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D004789:Enzyme Activation / Q000187:drug effects; D047348:Hydrolyzable Tannins / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides; D008168:Lung / Q000276:immunology / Q000473:pathology; D008264:Macrophages / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000378:metabolism; D020556:Neutrophil Infiltration / Q000187:drug effects / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D009195:Peroxidase / Q000378:metabolism; D011654:Pulmonary Edema / Q000188:drug therapy*; D011897:Random Allocation; D012128:Respiratory Distress Syndrome / Q000188:drug therapy*; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D047348:Hydrolyzable Tannins; C587672:IL1B protein, mouse; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; C115642:punicalagin; D009195:Peroxidase