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Preventive effects of edaravone, a free radical scavenger, on lipopolysaccharide‐induced lung injury in mice
Author(s) -
TAJIMA Shunji,
SODA Manabu,
BANDO Masashi,
ENOMOTO Munehiro,
YAMASAWA Hideaki,
OHNO Shoji,
TAKADA Toshinori,
SUZUKI Eiichi,
GEJYO Fumitake,
SUGIYAMA Yukihiko
Publication year - 2008
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/j.1440-1843.2008.01322.x
Subject(s) - edaravone , free radical scavenger , medicine , pharmacology , lipopolysaccharide , alveolar macrophage , oxidative stress , tumor necrosis factor alpha , reactive oxygen species , cytokine , immunology , pulmonary fibrosis , pathology , fibrosis , macrophage , in vitro , chemistry , biochemistry
Background and objective:  Reactive 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. Methods:  For 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. Results:  In the LPS‐induced ALI mouse model, the administration of edaravone attenuated cellular infiltration into and the concentrations of albumin, IL‐6, tumour necrosis factor‐α, 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. Conclusions:  In 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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