Eugenol attenuates pulmonary damage induced by diesel exhaust particles
Contribuinte(s) |
UNIVERSIDADE DE SÃO PAULO |
---|---|
Data(s) |
05/11/2013
05/11/2013
2012
|
Resumo |
Zin WA, Silva AG, Magalhaes CB, Carvalho GM, Riva DR, Lima CC, Leal-Cardoso JH, Takiya CM, Valen a SS, Saldiva PH, Faffe DS. Eugenol attenuates pulmonary damage induced by diesel exhaust particles. J Appl Physiol 112: 911-917, 2012. First published December 22, 2011; doi: 10.1152/japplphysiol.00764.2011.-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 mu l in; CTRL group) or 15 mu g of diesel particles DEP (15 mu g in; DIE and DEUG groups). After 1 h, mice received saline (10 mu l; CTRL and DIE groups) or eugenol (164 mg/kg; EUG and DEUG group) by gavage. Twenty-four hours after gavage, pulmonary resistive (Delta P1), viscoelastic (Delta P2) and total (Delta Ptot) pressures, static elastance (Est), and viscoelastic component of elastance (Delta E) 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, Delta P2, Delta Ptot, and Delta E 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. MCT/FAPERJ MCT/FAPERJ Brazilian Council for Scientific and Technological Development (CNPq) Brazilian Council for Scientific and Technological Development (CNPq) Carlos Chagas Filho Rio de Janeiro State Research Supporting Foundation (FAPERJ) Carlos Chagas Filho Rio de Janeiro State Research Supporting Foundation (FAPERJ) |
Identificador |
JOURNAL OF APPLIED PHYSIOLOGY, BETHESDA, v. 112, n. 5, supl. 2, Part 3, pp. 911-917, MAR, 2012 8750-7587 http://www.producao.usp.br/handle/BDPI/41378 10.1152/japplphysiol.00764.2011 |
Idioma(s) |
eng |
Publicador |
AMER PHYSIOLOGICAL SOC BETHESDA |
Relação |
JOURNAL OF APPLIED PHYSIOLOGY |
Direitos |
closedAccess Copyright AMER PHYSIOLOGICAL SOC |
Palavras-Chave | #APOPTOSIS #DIESEL EXHAUST PARTICLES #EUGENOL #INFLAMMATION #LUNG MECHANICS #OXIDATIVE STRESS #ALVEOLAR PRESSURE MEASUREMENT #KAPPA-B ACTIVATION #CYTOKINE EXPRESSION #LIPID-PEROXIDATION #PARTICULATE MATTER #OXIDATIVE STRESS #IN-VIVO #MICE #SYSTEM #RATS #PHYSIOLOGY #SPORT SCIENCES |
Tipo |
article original article publishedVersion |