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Anisomycin protects against sepsis by attenuating IリB kinase-dependent NF-リB activation and inflammatory gene expression
Gyoung Lim Park1,4 (Student), Minkyung Park1,4 (Student), Jeong-Ki Min2,4 (professor), Young-Jun Park1,4 (professor), Su Wol Chung3 (professor), Seon-Jin Lee 1,4,* (Professor)
1Environmental Disease Research Center and 2Biotherapeutics Translational Research Center, Korea Research Institute of Bioscience and Biotechnology,
3School of Biological Sciences, University of Ulsan,
4Department of Functional Genomics, University of Science and Technology
Anisomycin is known to inhibit eukaryotic protein synthesis and has been established as an antibiotic and anticancer drug. However, the molecular targets of anisomycin and its mechanism of action have not been elucidated in macrophages. Here, we investigated the anti-inflammatory effects of anisomycin both in vivo and in vitro. We found that anisomycin decreased the mortality rate of macrophages in models of cecal ligation and puncture (CLP)- and lipopolysaccharide (LPS)-induced acute sepsis. It also downregulated the gene expression of proinflammatory mediators, such as inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-メ, and interleukin-1モ, as well as the production of nitric oxide and proinflammatory cytokines in macrophages subjected to LPS-induced acute sepsis. Furthermore, in LPS-stimulated macrophages, anisomycin attenuated nuclear factor (NF)-リB activation, which is correlated with the inhibition of phosphorylation of NF-リB-inducing kinase and IリB kinase, phosphorylation and proteolytic degradation of IリBメ, and nuclear translocation of NF-リB p65 subunit. These results suggest that anisomycin prevents acute inflammation by inhibiting NF-リB-related inflammatory gene expression and is a potential therapeutic candidate for sepsis.
Abstract, Accepted Manuscript(in press) [Submitted on May 12, 2021, Accepted on June 24, 2021]
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