期刊
MOLECULES
卷 26, 期 17, 页码 -出版社
MDPI
DOI: 10.3390/molecules26175351
关键词
6-methylcoumarin; macrophage; inflammation; NF-kappa B; MAPK; coumarin
资金
- Jeju National University
The study demonstrated that 6-MC reduced the levels of nitric oxide and prostaglandin E-2 without causing cytotoxicity, and also decreased the expression of pro-inflammatory cytokines in a concentration-dependent manner in LPS-stimulated cells. Western blot results showed that 6-MC treatment decreased the protein levels of iNOS and COX-2 induced by LPS, while mechanistic studies revealed its inhibitory effects on the MAPK and NF-kappa B pathways.
Persistent inflammatory reactions promote mucosal damage and cause dysfunction, such as pain, swelling, seizures, and fever. Therefore, in this study, in order to explore the anti-inflammatory effect of 6-methylcoumarin (6-MC) and suggest its availability, macrophages were stimulated with lipopolysaccharide (LPS) to conduct an in vitro experiment. The effects of 6-MC on the production and levels of pro-inflammatory cytokines (interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha) and inflammatory mediators (nitric oxide (NO), prostaglandin E-2 (PGE(2))) in LPS-stimulated RAW 264.7 cells were examined. The results showed that 6-MC reduced the levels of NO and PGE(2) without being cytotoxic. In addition, it was demonstrated that the increase in the expression of pro-inflammatory cytokines caused by LPS stimulation, was decreased in a concentration-dependent manner with 6-MC treatment. Moreover, Western blot results showed that the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), which increased with LPS treatment, were decreased by 6-MC treatment. Mechanistic studies revealed that 6-MC reduced the phosphorylation of the mitogen-activated protein kinase (MAPK) family and I kappa B alpha in the MAPK and nuclear factor-kappa B (NF-kappa B) pathways, respectively. These results suggest that 6-MC is a potential therapeutic agent for inflammatory diseases that inhibits inflammation via the MAPK and NF-kappa B pathways.
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