Journal
TOXICOLOGY AND APPLIED PHARMACOLOGY
Volume 285, Issue 2, Pages 128-135Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2015.04.004
Keywords
Acteoside; Lipopolysaccharide (LPS); Lung injury; Nuclear factor-kappa B (NF-kappa B); Lung epithelial cells; Mice
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The purpose of the present study was to investigate the protective role of acteoside (AC) on lipopolysaccharide (LPS)-induced acute lung injury (ALL). BalB/c mice intraperitoneally received AC (30, and 60 mg/kg) or dexamethasone (2 mg/kg) 2 h prior toot 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-alpha (TNF-alpha),interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) in LPS-stimulated mice. Furthermore, we demonstrated that AC inhibited the phosphorylation of I kappa B alpha, nuclear factor-kappa B (NF-kappa B) p65, inhibitor of nuclear factor kappa-B kinase-alpha (IKK-alpha) and inhibitor of nuclear factor kappa-B kinase-beta (IKK beta) 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-kappa B activation. (C) 2015 Elsevier Inc. All rights reserved.
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