Abstract
We investigated the effects and associated mechanism of alkannin (AL) on lipopolysaccharide (LPS)-induced acute lung injury in a mouse model. Pretreatment with AL in vivo significantly reduced the lung wet/dry weight ratio and inhibited lung myeloperoxidase activity and malondialdehyde content, while increasing superoxide dismutase activity. Hematoxylin and eosin staining demonstrated that AL attenuated lung histopathological changes. In addition, AL-inhibited overproduction of proinflammatory cytokines in bronchoalveolar lavage fluid and lung tissues in LPS-injured mice and LPS-exposed A549 cells. Further analysis showed that AL-inhibited induction of the Rho/ROCK/NF-κB pathway via LPS-induced inflammation in mice and A549 cells. Fasudil, a selective ROCK inhibitor, showed similar effects. Overall, the findings indicate that AL suppresses the expression of messenger RNAs and proteins associated with Rho/ROCK/NF-κB signaling to effectively ameliorate lung injury.
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