Cargando…

Carnosic acid protects against lipopolysaccharide-induced acute lung injury in mice

Acute respiratory distress syndrome is a well-known inflammatory disease associated with high rates of morbidity and mortality due to a lack of effective treatment methods. Carnosic acid (CA) is a phenolic diterpene compound that serves a central role in cytoprotective responses to inflammation. In...

Descripción completa

Detalles Bibliográficos
Autores principales: Li, Quan, Liu, Ling, Sun, Haijun, Cao, Kunyue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781802/
https://www.ncbi.nlm.nih.gov/pubmed/31611929
http://dx.doi.org/10.3892/etm.2019.8042
_version_ 1783457444272275456
author Li, Quan
Liu, Ling
Sun, Haijun
Cao, Kunyue
author_facet Li, Quan
Liu, Ling
Sun, Haijun
Cao, Kunyue
author_sort Li, Quan
collection PubMed
description Acute respiratory distress syndrome is a well-known inflammatory disease associated with high rates of morbidity and mortality due to a lack of effective treatment methods. Carnosic acid (CA) is a phenolic diterpene compound that serves a central role in cytoprotective responses to inflammation. In the present study, the protective mechanism of CA on acute lung injury (ALI) induced by lipopolysaccharide (LPS) was investigated. Mice were randomly assigned to the following five groups: Control group, LPS group, and LPS plus CA groups (at 10, 20 and 40 mg/kg doses). Following pre-treatment with vehicle or CA, ALI was induced by the administration of LPS. At 6 h after LPS treatment, mice were sacrificed and lung tissues were harvested for histologic analysis and the determination of wet-to-dry ratio, myeloperoxidase activity and toll-like receptor 4 (TLR4) and NF-κB expression. Additionally, the levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) were determined in bronchoalveolar lavage fluid (BALF) and lung tissues, as well as the rate of apoptosis of the isolated neutrophils from BALF. The alleviation of LPS-induced ALI by CA was confirmed by histologic results and a reduction in the wet-to-dry ratio of lung tissues. Additionally, CA was revealed to significantly suppress the inhibitory effect of LPS on neutrophil apoptosis and the promoting effects of LPS on IL-1β, IL-6, TNF-α, TLR4 and NF-κB expression, and NF-κB phosphorylation. The current results indicated that CA protects against LPS-induced ALI via a mechanism that inhibits inflammation.
format Online
Article
Text
id pubmed-6781802
institution National Center for Biotechnology Information
language English
publishDate 2019
publisher D.A. Spandidos
record_format MEDLINE/PubMed
spelling pubmed-67818022019-10-14 Carnosic acid protects against lipopolysaccharide-induced acute lung injury in mice Li, Quan Liu, Ling Sun, Haijun Cao, Kunyue Exp Ther Med Articles Acute respiratory distress syndrome is a well-known inflammatory disease associated with high rates of morbidity and mortality due to a lack of effective treatment methods. Carnosic acid (CA) is a phenolic diterpene compound that serves a central role in cytoprotective responses to inflammation. In the present study, the protective mechanism of CA on acute lung injury (ALI) induced by lipopolysaccharide (LPS) was investigated. Mice were randomly assigned to the following five groups: Control group, LPS group, and LPS plus CA groups (at 10, 20 and 40 mg/kg doses). Following pre-treatment with vehicle or CA, ALI was induced by the administration of LPS. At 6 h after LPS treatment, mice were sacrificed and lung tissues were harvested for histologic analysis and the determination of wet-to-dry ratio, myeloperoxidase activity and toll-like receptor 4 (TLR4) and NF-κB expression. Additionally, the levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) were determined in bronchoalveolar lavage fluid (BALF) and lung tissues, as well as the rate of apoptosis of the isolated neutrophils from BALF. The alleviation of LPS-induced ALI by CA was confirmed by histologic results and a reduction in the wet-to-dry ratio of lung tissues. Additionally, CA was revealed to significantly suppress the inhibitory effect of LPS on neutrophil apoptosis and the promoting effects of LPS on IL-1β, IL-6, TNF-α, TLR4 and NF-κB expression, and NF-κB phosphorylation. The current results indicated that CA protects against LPS-induced ALI via a mechanism that inhibits inflammation. D.A. Spandidos 2019-11 2019-09-23 /pmc/articles/PMC6781802/ /pubmed/31611929 http://dx.doi.org/10.3892/etm.2019.8042 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by-nc/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Li, Quan
Liu, Ling
Sun, Haijun
Cao, Kunyue
Carnosic acid protects against lipopolysaccharide-induced acute lung injury in mice
title Carnosic acid protects against lipopolysaccharide-induced acute lung injury in mice
title_full Carnosic acid protects against lipopolysaccharide-induced acute lung injury in mice
title_fullStr Carnosic acid protects against lipopolysaccharide-induced acute lung injury in mice
title_full_unstemmed Carnosic acid protects against lipopolysaccharide-induced acute lung injury in mice
title_short Carnosic acid protects against lipopolysaccharide-induced acute lung injury in mice
title_sort carnosic acid protects against lipopolysaccharide-induced acute lung injury in mice
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781802/
https://www.ncbi.nlm.nih.gov/pubmed/31611929
http://dx.doi.org/10.3892/etm.2019.8042
work_keys_str_mv AT liquan carnosicacidprotectsagainstlipopolysaccharideinducedacutelunginjuryinmice
AT liuling carnosicacidprotectsagainstlipopolysaccharideinducedacutelunginjuryinmice
AT sunhaijun carnosicacidprotectsagainstlipopolysaccharideinducedacutelunginjuryinmice
AT caokunyue carnosicacidprotectsagainstlipopolysaccharideinducedacutelunginjuryinmice