| Literature DB >> 30924981 |
Bin Li1, Qingling Lin1, Qiliang Hou1, Chao Yin1, Lei Zhang1, Yumin Li1.
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.Entities:
Keywords: Rho/ROCK/NF-κB; alkannin; lipopolysaccharide; lung injury
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Year: 2019 PMID: 30924981 DOI: 10.1002/jbt.22323
Source DB: PubMed Journal: J Biochem Mol Toxicol ISSN: 1095-6670 Impact factor: 3.642