Article Sidebar
Published:
Jul 20, 2021Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Usnic acid ameliorates bleomycin-induced pulmonary fibrosis in mice via inhibition of inflammatory responses and oxidative stress
Abstract
Purpose: To Investigate the effect of usnic acid (UA) on bleomycin (BLM)-induced pulmonary fibrosis in mice, and the underlying mechanism.
Methods: Male Kunming mice with bleomycin-induced pulmonary fibrosis (PF) were exposed to different concentrations of usnic acid. Lung coefficient and histopathological changes were determined, while MDA, superoxide dismutase (SOD) activity, and expression levels of hydroxyproline, tumor necrosis factor-α, interleukins-1β & 6, and transforming growth factor-β1 were assayed in lung homogenates.
Results: UA significantly mitigated lung coefficient and histopathological changes in mice. Compared to the bleomycin group, MDA level was significantly reduced while the content of SOD markedly increased after UA pretreatment (p < 0.05). Moreover, UA significantly reduced the expression levels of all the parameters, relative to bleomycin group (p < 0.05).
Conclusion: These results indicate that UA protects mice against bleomycin-induced PF via a mechanism associated with attenuation of pro-oxidant stress and inflammation. Therefore, UA has therapeutic potential for the management of pulmonary fibrosis.
