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Tectorigenin (Tg) and tectoridin (Td) are the major compounds isolated from the rhizomes of iridaceous plant Belamcanda chinensis which is well known as a chinese traditional medicine for the treatment of inflammatory diseases. In this study we investigated whether tectorigenin and tectoridin can be applied to the suppression of interferon-gamma and lipopolysaccharide (IFN-gamma/LPS)-induced inflammatory responses in macrophages. Anti-inflammatory activities of tectorigenin and tectoridin were compared with genistein (Ge), well known isoflavonoid as a phytoestrogen and regarded as an emerging anti-inflammatory agent. Both compounds showed low cytotoxic effect. In Raw 264.7 cells activated with IFN-gamma/LPS, pre-treated tectorigenin was found to inhibit the expression of inducible nitric oxide synthase (iNOS), the production of nitric oxide (NO) and the secretion of interleukin (IL)-1beta dose-dependently. Tectorigenin also decreased the expression of cyclooxigenase (COX)-2 and the production of prostaglandin E(2) (PGE(2)) in dose-dependent manner. These inhibitory effects of tectorigenin were found to be caused by the blocking of nuclear factor kappa-B (NF-kappaB) activation. Compared with genistein and tectoridin, tectorigenin showed significant inhibitory effect for almost anti-inflammatory tests in this study. All these results clearly demonstrated that tectorigenin appears to have the potential to prevent inflammation.

Flavonoids have biological activities including anti-allergic, anti-inflammatory, antimicrobial and anticancer activities shown from in vitro studies. Of these biological activities, the anti-inflammatory capacity of flavonoids has long been emphasized in Chinese medicine. In this study, I investigated that what flavonoid can be applied to the suppression of lipopolysaccharide (LPS)-induced inflammatory responses in macrophages among the four similar structure flavonoids. Eriodictyol was found to reduce nitric oxide (NO) production from LPS-stimulated Raw 264.7 cells in non-cytotoxic concentrations. Moreover, eriodictyol strongly suppressed the phagocytic activity of activated macrophages. Pre-treatment of Raw 264.7 cells with eriodictyol reduced the expression of mRNA and the secretion of pro-inflammatory cytokines. These inhibitory effects were found to be caused by blockage of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinase (JNK).