Acute lung injury (ALI) is a serious disease with unacceptably high mortality and
morbidity rates. Up to now, no effective therapeutic strategy for ALI has been established.
Rutin, quercetin-3-rhamnosyl glucoside, expresses a wide range of biological activities
and pharmacological effects, such as anti-inflammatory, antihypertensive, anticarcinogenic,
vasoprotective, and cardioprotective activities. Pretreatment with rutin inhibited
not only histopathological changes in lung tissues but also infiltration of polymorphonuclear
granulocytes into bronchoalveolar lavage fluid in lipopolysaccharide (LPS)-induced
ALI. In addition, LPS-induced inflammatory responses, including increased secretion
of proinflammatory cytokines and lipid peroxidation, were inhibited by rutin in a
concentration-dependent manner. Furthermore, rutin suppressed phosphorylation of NF-κB
and MAPK and degradation of IκB, an NF-κB inhibitor. Decreased activities of antioxidative
enzymes such as superoxide dismutase, catalase, glutathione peroxidase, and heme oxygenase-1
caused by LPS were reversed by rutin. At the same time, we found that ALI amelioration
by chelation of extracellular metal ions with rutin is more efficacious than with
deferoxamine. These results indicate that the protective mechanism of rutin is through
inhibition of MAPK-NF-κB activation and upregulation of antioxidative enzymes.
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