Anisomycin protects against sepsis by attenuating IκB kinase-dependent NF-κB activation and inflammatory gene expression

• Published in: BMB reports Vol. 54; no. 11; pp. 545 - 550
• Main Authors: Park, Gyoung Lim, Park, Minkyung, Min, Jeong-Ki, Park, Young-Jun, Chung, Su Wol, Lee, Seon-Jin
• Format: Journal Article
• Language: English
• Published: Korea (South) Korean Society for Biochemistry and Molecular Biology 30.11.2021; 생화학분자생물학회
• Subjects: Animals; Anisomycin - pharmacology; Female; Gene Expression Regulation - drug effects; I-kappa B Proteins - antagonists & inhibitors; I-kappa B Proteins - genetics; I-kappa B Proteins - metabolism; Inflammation - etiology; Inflammation - metabolism; Inflammation - pathology; Inflammation - prevention & control; Inflammation Mediators - metabolism; Lipopolysaccharides - toxicity; Mice; Mice, Inbred C57BL; NF-kappa B - antagonists & inhibitors; Nitric Oxide - metabolism; Protein Synthesis Inhibitors - pharmacology; Sepsis - chemically induced; Sepsis - metabolism; Sepsis - pathology; Sepsis - prevention & control; 화학

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 explained in macrophages. Here, we demonstrated the anti-inflammatory effects of anisomyci...