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Acute lung injury (ALI), the causative factor for acute respiratory distress   syndrome, results in significant morbidity and mortality. Due to a lack of   effective therapeutic options for ALI, the development of novel therapies is   urgently needed. NF-κB, an inflammatory mediator necessary for the evolution   of ALI, could serve as an important target for novel agents to prevent   disease progression. The present study was designed to evaluate the   protective effect of 6-shogaol against lipopolysaccharide (LPS)-induced ALI   in mice, and its mechanism of action. Our results suggest that 6-shogaol   significantly attenuates elevated levels of various proinflammatory   cytokines, such as tumor necrosis factor alpha (TNFα), IL-1β and IL-6.   Moreover, the influx of neutrophils, increased protein concentration and   edema were also suppressed in mice pretreated with 6-shogaol. These   observations were also confirmed by histopathological examination of lung   tissues, which suggests that 6-shogaol significantly improves the   pathological condition to normal in a dose-dependent manner. A docking study   of 6-shogaol was also performed, with the NF-κB p50 homodimer bound to a κB   site, to determine its possible inhibitory effects. Our results show that   6-shogaol was efficiently accommodated in the deep cleft of the active site,   lined with residues Tyr57, Val58 and Cys59, Tyr143, Lys145 and Lys146 of   Chain B of p50 NF-κB

Examination of the protective effect of 6-shogaol against LPS-induced acute lung injury in mice via NF-kB attenuation