Eugenol attenuates pulmonary damage induced by diesel exhaust particles


Autoria(s): Zin, Walter A.; Silva, Ana G. L. S.; Magalhaes, Clarissa B.; Carvalho, Giovanna M. C.; Riva, Douglas R.; Lima, Crystianne C.; Leal-Cardoso, Jose H.; Takiya, Christina M.; Valenca, Samuel S.; Saldiva, Paulo H. N.; Faffe, Debora S.
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

http://dx.doi.org/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