| 20075264 |
Magalhaes CB, Riva DR, Depaula LJ, Brando-Lima AC, Koatz VL, Leal-Cardoso JH, Zin WA, Faffe DS: In vivo anti-inflammatory action of eugenol on lipopolysaccharide-induced lung injury. J Appl Physiol. 2010 Jan 14.
Eugenol, a methoxyphenol component of clover oil, suppresses cyclooxygenase-2 expression, while eugenol dimers prevent nuclear factor kappa B activation and inflammatory cytokine expression in lipopolysaccharide-stimulated macrophages. Our aim was to examine the in vivo anti-inflammatory effects of eugenol. BALB/c mice were divided into 3 groups. Mice received saline (0.05 mL i.t., CTRL group) or E. coli LPS (10 mug i.t., LPS and LPSEUG groups). After 6 h, mice received saline (0.2 mL i.p., CTRL and LPS groups) or eugenol (160 mg.kg (-1) i.p., LPSEUG group). Twenty four hours after LPS injection, pulmonary resistive (DeltaP1) and viscoelastic (DeltaP2) pressures, static elastance (Est) and viscoelastic component of elastance (DeltaE) were measured. Lungs were prepared for histology. In parallel mice, BALF was collect 24 h after LPS injection. TNF-alpha was determined by ELISA. Lung tissue expression of NF-kappaB was determined by EMSA. DeltaP1, DeltaP2, Est and DeltaE were significantly higher in LPS than in the other groups. LPS also showed significantly more alveolar collapse, collagen fibers, neutrophil influx, higher TNF-alpha levels and NF-kappaB expression than the other groups. Eugenol treatment reduced LPS-induced lung inflammation, improving lung function. Our results suggest that eugenol exhibits in vivo anti-inflammatory action in LPS-induced lung injury. Key words: acute lung injury, inflammation, lipopolysaccharide, lung mechanics. |
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