• Shunji Tajima, Manabu Soda, Masashi Bando, Munehiro Enomoto, Hideaki Yamasawa, Shoji Ohno, Toshinori Takada, Eiichi Suzuki, Fumitake Gejyo, and Yukihiko Sugiyama.
• Department of Medicine, Division of Pulmonary Medicine, Jichi Medical University, Tochigi, Japan. tajimash@med.niigata-u.ac.jp
• Respirology. 2008 Sep 1;13(5):646-53.

Background And ObjectiveReactive oxygen species (ROS) play an important role in the pathogenesis of acute lung injury (ALI) and pulmonary fibrosis. It was hypothesized that edaravone, a free radical scavenger, would be able to attenuate LPS-induced lung injury in mice by decreasing oxidative stress.MethodsFor the in vivo experiments, lung injury was induced in female BALB/c mice by the intranasal instillation of LPS. Edaravone was given by intraperitoneal administration 1 h before the LPS challenge. For the in vitro experiments, MH-S cells (murine alveolar macrophage cell line) were exposed to edaravone, followed by stimulation with LPS.ResultsIn the LPS-induced ALI mouse model, the administration of edaravone attenuated cellular infiltration into and the concentrations of albumin, IL-6, tumour necrosis factor-alpha, keratinocyte-derived chemokine and macrophage inflammatory protein-2 in BAL fluid. In addition, the in vitro studies showed that the elevated IL-6 secretion from MH-S cells in response to LPS was significantly attenuated by co-incubation with edaravone.ConclusionsIn an experimental murine model, a free radical scavenger may prevent ALI via repression of pro-inflammatory cytokine production by lung macrophages.

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