title: Eugenol attenuates pulmonary damage induced by diesel exhaust particles.
abstract: Environmentally relevant doses of inhaled diesel particles elicit pulmonary inflammation and impair lung mechanics. Eugenol, a methoxyphenol component of clove oil, presents in vitro and in vivo anti-inflammatory and antioxidant properties. Our aim was to examine a possible protective role of eugenol against lung injuries induced by diesel particles. Male BALB/c mice were divided into four groups. Mice received saline (10 μl in; CTRL group) or 15 μg of diesel particles DEP (15 μg in; DIE and DEUG groups). After 1 h, mice received saline (10 μl; CTRL and DIE groups) or eugenol (164 mg/kg; EUG and DEUG group) by gavage. Twenty-four hours after gavage, pulmonary resistive (ΔP1), viscoelastic (ΔP2) and total (ΔPtot) pressures, static elastance (Est), and viscoelastic component of elastance (ΔE) were measured. We also determined the fraction areas of normal and collapsed alveoli, amounts of polymorpho- (PMN) and mononuclear cells in lung parenchyma, apoptosis, and oxidative stress. Est, ΔP2, ΔPtot, and ΔE were significantly higher in the DIE than in the other groups. DIE also showed significantly more PMN, airspace collapse, and apoptosis than the other groups. However, no beneficial effect on lipid peroxidation was observed in DEUG group. In conclusion, eugenol avoided changes in lung mechanics, pulmonary inflammation, and alveolar collapse elicited by diesel particles. It attenuated the activation signal of caspase-3 by DEP, but apoptosis evaluated by TUNEL was avoided. Finally, it could not avoid oxidative stress as indicated by malondialdehyde.
authors.affiliation: Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. wazin@biof.ufrj.br
authors.forename: Walter A
authors.initials: WA
authors.lastname: Zin
authors.forename: Ana G L S
authors.initials: AG
authors.lastname: Silva
authors.forename: Clarissa B
authors.initials: CB
authors.lastname: Magalhães
authors.forename: Giovanna M C
authors.initials: GM
authors.lastname: Carvalho
authors.forename: Douglas R
authors.initials: DR
authors.lastname: Riva
authors.forename: Crystianne C
authors.initials: CC
authors.lastname: Lima
authors.forename: Jose H
authors.initials: JH
authors.lastname: Leal-Cardoso
authors.forename: Christina M
authors.initials: CM
authors.lastname: Takiya
authors.forename: Samuel S
authors.initials: SS
authors.lastname: Valença
authors.forename: Paulo H N
authors.initials: PH
authors.lastname: Saldiva
authors.forename: Débora S
authors.initials: DS
authors.lastname: Faffe
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D005054:Eugenol / Q000494:pharmacology*; D020287:In Situ Nick-End Labeling / Q000379:methods; D015227:Lipid Peroxidation / Q000187:drug effects; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018384:Oxidative Stress / Q000187:drug effects; D010316:Particle Size; D011014:Pneumonia / Q000139:chemically induced* / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D011650:Pulmonary Alveoli / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D015656:Respiratory Mechanics / Q000187:drug effects; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D001335:Vehicle Emissions; D005054:Eugenol; D053148:Caspase 3