The anti-inflammatory and anti-oxidative actions of eugenol improve lipopolysaccharide-induced lung injury.

Acute lung injury (ALI) remains a major cause of mortality. In lipopolysaccharide (LPS)-stimulated macrophages, eugenol reduces cyclooxygenase-2 expression, NF-κB 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.

Eugenol attenuates pulmonary damage induced by diesel exhaust particles.

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.

Lipopolysaccharide-induced lung injury: role of P2X7 receptor.

Rationale: P2X7 receptors have been involved in inflammatory and immunological responses, and their activation modulates pro-inflammatory cytokines production by LPS-challenged macrophages.

Objectives: To determine the role of P2X7R in LPS-induced acute lung injury in mice.

Methods: Wild-type (C57BL/6) and P2X7 knockout mice received intratracheal injection of saline or Escherichia coli LPS (60 μg).

In vivo anti-inflammatory action of eugenol on lipopolysaccharide-induced lung injury.

Eugenol, a methoxyphenol component of clove oil, suppresses cyclooxygenase-2 expression, while eugenol dimers prevent nuclear factor-kappaB (NF-kappaB) 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 four groups.

Recruitment maneuver in pulmonary and extrapulmonary experimental acute lung injury.

Objective: The aim of this study is to test the hypothesis that recruitment maneuvers (RMs) might act differently in models of pulmonary (p) and extrapulmonary (exp) acute lung injury (ALI) with similar transpulmonary pressure changes.

Design: Prospective, randomized, controlled experimental study.

Setting: University research laboratory.