Salicortin suppresses lipopolysaccharide-stimulated inflammatory responses via blockade of NF-κB and JNK activation in RAW 264.7 macrophages

• Published in: BMB reports Vol. 47; no. 6; pp. 318 - 323
• Main Authors: Kwon, Dong-Joo, Bae, Young-Soo, Ju, Sung Mi, Youn, Gi Soo, Choi, Soo Young, Park, Jinseu
• Format: Journal Article
• Language: English
• Published: Korea (South) Korean Society for Biochemistry and Molecular Biology 01.06.2014; 생화학분자생물학회
• Subjects: Animals; Anti-Inflammatory Agents - pharmacology; Cell Line; Cytokines - metabolism; Glucosides - pharmacology; I-kappa B Proteins - metabolism; JNK Mitogen-Activated Protein Kinases - metabolism; Lipopolysaccharides - toxicity; Macrophages - cytology; Macrophages - drug effects; Macrophages - metabolism; Mice; NF-kappa B - antagonists & inhibitors; NF-kappa B - metabolism; NF-KappaB Inhibitor alpha; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - metabolism; Phosphorylation - drug effects; Plant Bark - metabolism; Plant Extracts - chemistry; Plant Extracts - pharmacology; Populus - metabolism; Signal Transduction - drug effects; Transcription Factor RelA - metabolism; 화학
• ISSN: 1976-6696; 1976-670X
• DOI: 10.5483/BMBRep.2014.47.6.200

We isolated the phenolic glucoside salicortin from a Populus euramericana bark extract, and examined its ability to suppress inflammatory responses as well as the molecular mechanisms underlying these abilities, using lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Salicortin inhibited iNOS expression and the subsequent production of NO in a dose-dependent manner in the LPS-stimulated RAW 264.7 cells. Salicortin significantly suppressed LPS-induced signal cascades of NF-κB activation, such as IKK activation, IκBα phosphorylation and p65 phosphorylation in RAW 264.7 cells. In addition, salicortin inhibited the LPS-induced activation of JNK, but not ERK or p38 MAPK. Furthermore, salicortin significantly inhibited production of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 in the LPS-stimulated RAW 264.7 cells. These findings suggest that salicortin may show its anti-inflammatory activity by suppressing the LPS-induced expression of pro-inflammatory mediators through inhibition of NF-κB and JNK MAPK signaling cascades in macrophages.