Journal
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
Volume 259, Issue -, Pages 30-36Publisher
ELSEVIER
DOI: 10.1016/j.resp.2018.07.001
Keywords
Acute lung injury; Oxidative stress; Pulmonary inflammation; Lipopolysaccharide; Lung mechanic
Categories
Funding
- Centers of Excellence Program (PRONEX-MCTI/FAPERJ) [E-26/110.575/2010]
- Brazilian Council for Scientific and Technological Development (CNPq) [470495/2012-0, 300531/2012-5]
- Carlos Chagas Filho Rio de Janeiro State Research Supporting Foundation (FAPERJ) [E-26/103.184/2011, E-26/201.450/2014]
Ask authors/readers for more resources
Acute lung injury (ALI) remains a major cause of mortality. In lipopolysaccharide (LPS)-stimulated macrophages, eugenol reduces cyclooxygenase-2 expression, NF-KB activation, and inflammatory mediators. We examined the anti-inflammatory and anti-oxidative action of eugenol in an in vivo model of LPS-induced lung injury. Lung mechanics and histology were analyzed in mice 24 h after LPS exposure, with and without eugenol treatment at different doses. Additional animals, submited to the same protocol, were treated with eugenol at 150 mg/kg to determine its effect on inflammatory cytokines (ELISA) and oxidative markers. LPS-induced lung functional and histological changes were significantly improved by eugenol, in a dose-dependent way. Furthermore, eugenol (150 mg/kg) was able to inhibit the release of inflammatory cytokines (TNF-alpha, IL-1 beta and IL-6), NADPH oxidase activity, as well as antioxidant enzymes activity (superoxide dismutase, catalase and glutathione peroxidase). Finally, eugenol reduced LPS-induced protein oxidation. In conclusion, eugenol improved in vivo LPS-induced ALI through both anti-inflammatory and anti-oxidative effects, avoiding damage to lung structure.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available