Nitric oxide (NO) and prostaglandin (PG)E2, known inflammatory mediators, are critically involved in the pathogenesis of a large number of human inflammatory diseases. Therefore, a search of inducible nitric oxide synthases (iNOS) and cyclooxygenase 2 (COX-2) selective inhibitors is a useful strategy to find functional substances to alleviate inflammatory disease. In our search for anti-inflammatory ingredients, we found that extracts of Ulva fasciata (UFE) and Desmarestia viridis (DVE) inhibit the generation of NO and PGE2 in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. U. fasciata and D. viridis were extracted with 80% ethanol and then partitioned successively with ethyl acetate. The ethyl acetate fractions are effective dose-dependent inhibitors of LPS-induced NO and PGE2 synthesis in RAW 264.7 cells. To test the inhibitory effects of UFE and DVE on pro-inflammatory cytokines, we performed ELISA assays for tumor necrosis factor (TNF)-α, IL (interleukin)-1β, and IL(interleukin)-6 in LPS-stimulated RAW 264.7 macrophage cells. In these assays, the UFE and DVE showed a dose-dependent decrease in the production of TNF-α, IL-1β, and IL-6. As a preliminary study of the anti-inflammatory mechanism, we determined, using the Western blot analysis, whether or not UFE and DVE inhibit the degradation of I-kappa-B-alpha (IKB-α). Our results indicate that UFE and DVE indeed prevent the degradation of IKB-α, in a dose-dependent manner. Based on these results, we suggest that extracts of U. fasciata and D. viridis be considered candidates for anti-inflammatory agents for human use. © 2013 Min-Jin Kim et al.
CITATION STYLE
Kim, M. J., Yang, K. W., Lee, W. J., Kim, S. S., Ho Lee, N., & Hyun, C. G. (2013). Inhibitory effect of ulva fasciata and desmarestia viridis on the production of Nitric oxide, prostaglandin E2, and pro-inflammatory cytokines in RAW 264.7 cells. Journal of Applied Pharmaceutical Science, 3(9), 1–7. https://doi.org/10.7324/JAPS.2013.3901
Mendeley helps you to discover research relevant for your work.