title: Effects of acteoside on lipopolysaccharide-induced inflammation in acute lung injury via regulation of NF-κB pathway in vivo and in vitro.
abstract: The purpose of the present study was to investigate the protective role of acteoside (AC) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). BalB/c mice intraperitoneally received AC (30, and 60 mg/kg) or dexamethasone (2 mg/kg) 2h prior to or after intratracheal instillation of LPS. Treatment with AC significantly decreased lung wet-to-dry weight (W/D) ratio and lung myeloperoxidase (MPO) activity and ameliorated LPS-induced lung histopathological changes. In addition, AC increased super oxide dismutase (SOD) level and inhibited malondialdehyde (MDA) content, total cell and neutrophil infiltrations, and levels of proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) in LPS-stimulated mice. Furthermore, we demonstrated that AC inhibited the phosphorylation of IκBα, nuclear factor-κB (NF-κB) p65, inhibitor of nuclear factor kappa-B kinase-α (IKK-α) and inhibitor of nuclear factor kappa-B kinase-β (IKKβ) in LPS-induced inflammation in A549 cells. Our data suggested that LPS evoked the inflammatory response in lung epithelial cells A549. The experimental results indicated that the protective mechanism of AC might be attributed partly to the inhibition of proinflammatory cytokine production and NF-κB activation.
authors.affiliation: Changchun University of Chinese Medicine, Changchun 130117, China.
authors.forename: Wang
authors.initials: W
authors.lastname: Jing
authors.affiliation: Changchun University of Chinese Medicine, Changchun 130117, China. Electronic address: machunhuabest@126.com.
authors.forename: Ma
authors.initials: M
authors.lastname: Chunhua
authors.affiliation: Changchun University of Chinese Medicine, Changchun 130117, China. Electronic address: wangshuminch@126.com.
authors.forename: Wang
authors.initials: W
authors.lastname: Shumin
mesh_terms: D055371:Acute Lung Injury / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D016207:Cytokines / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D005960:Glucosides / Q000493:pharmacokinetics / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D008168:Lung / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000187:drug effects*; D010636:Phenols / Q000493:pharmacokinetics / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects; D013482:Superoxide Dismutase / Q000378:metabolism; D059808:Polyphenols
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D003907:Dexamethasone; D005960:Glucosides; D008070:Lipopolysaccharides; D008315:Malondialdehyde; D016328:NF-kappa B; D010636:Phenols; D013482:Superoxide Dismutase; C058956:acteoside; D059808:Polyphenols
keywords: Acteoside; Lipopolysaccharide (LPS); Lung epithelial cells; Lung injury; Mice; Nuclear factor-κB (NF-κB)