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- (-)-pinoresinol monomethyl ether inhibits LPS-induced iNOS and Cox-2 expression via the attenuation of NF-κb in Raw 264.7 macrophage cells
- B Y Park; M Y Lee; Kyung Seop Ahn; Y W Chin; Hyeong Kyu Lee; Sei Ryang Oh
- Bibliographic Citation
- Journal of Korean Society for Applied Biological Chemistry, vol. 54, no. 2, pp. 163-168
- Publication Year
- Anti-inflammatory effects of (-)-pinoresinol monomethyl ether (PME) were evaluated on lipopolysaccharide (LPS)-treated Raw 264.7 macrophage cells. PME inhibited translocation of p65-nuclear factor-κB (NF-κB) into the nucleus in immunocytochemical analysis for NF-κB activation, expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in Western blotting, as well as production of pro-inflammatory mediators, such as nitric oxide (NO), tumor necrosis factor (TNF-α), and prostaglandin E2 (PGE2) in LPS-induced Raw 264.7 cells. These results suggest the anti-inflammatory activity of PME could be due to the down-regulation of iNOS, COX-2, TNF-α, and PGE2 in activated Raw 264.7 cells through NF-κB-dependent pathways.
- (-)-pinoresinol monomethyl ether; Cox-2; Inducible nitric oxide synthase; Nitric oxide; Nuclear factor-κb; Prostaglandin e2; Tumor necrosis factor
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- Ochang Branch Institute > Natural Medicine Research Center > 1. Journal Articles
Ochang Branch Institute > 1. Journal Articles
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