CD （Cryptocarya densiflora） Blume has traditionally been used as an herbal medicine. In this study, the effects of CDEE （CD ethanol extract） on inflammation were investigated in LPS （lipopolysaccharide）-stimulat...CD （Cryptocarya densiflora） Blume has traditionally been used as an herbal medicine. In this study, the effects of CDEE （CD ethanol extract） on inflammation were investigated in LPS （lipopolysaccharide）-stimulated mouse RAW264.7 macrophages. We investigated the effects of CDEE on the production of NO, PGE2 interleukin （IL）-6, IL-1β, and tumor necrosis factor （TNF）-α in LPS-stimulated RAW264.7 cells. We measured the mRNA or protein expression of the pro-inflammatory mediators induced by CDEE in LPS-stimulated RAW264.7 cells. We explored the expression of Nrf-2, heme oxygenase （HO）-I and NADPH-quinone oxidoreductase （NQO）-I to elucidate the antioxidative mechanisms. CDEE significantly inhibited the production of NO, PGE2, IL-6, IL-1β and TNF-α in LPS-stimulated RAW264.7 cells. CDEE suppressed the mRNA or protein expression of iNOS, COX-2, and the MAPKs with a reduction in the translocation of NF-κB in LPS-stimulated RAW264.7 cells. In addition, CDEE significantly increased the expression of HO-I and NQO-1 with an increase in the translocation of Nrf-2 into the nucleus. These results indicate that CDEE inhibits the LPS-induced inflammatory and oxidative responses via suppression of NF-κB activation and the enhancement of Nrf2 activation. We suggest that CDEE may be therapeutic for treating inflammatory diseases.展开更多
文摘CD （Cryptocarya densiflora） Blume has traditionally been used as an herbal medicine. In this study, the effects of CDEE （CD ethanol extract） on inflammation were investigated in LPS （lipopolysaccharide）-stimulated mouse RAW264.7 macrophages. We investigated the effects of CDEE on the production of NO, PGE2 interleukin （IL）-6, IL-1β, and tumor necrosis factor （TNF）-α in LPS-stimulated RAW264.7 cells. We measured the mRNA or protein expression of the pro-inflammatory mediators induced by CDEE in LPS-stimulated RAW264.7 cells. We explored the expression of Nrf-2, heme oxygenase （HO）-I and NADPH-quinone oxidoreductase （NQO）-I to elucidate the antioxidative mechanisms. CDEE significantly inhibited the production of NO, PGE2, IL-6, IL-1β and TNF-α in LPS-stimulated RAW264.7 cells. CDEE suppressed the mRNA or protein expression of iNOS, COX-2, and the MAPKs with a reduction in the translocation of NF-κB in LPS-stimulated RAW264.7 cells. In addition, CDEE significantly increased the expression of HO-I and NQO-1 with an increase in the translocation of Nrf-2 into the nucleus. These results indicate that CDEE inhibits the LPS-induced inflammatory and oxidative responses via suppression of NF-κB activation and the enhancement of Nrf2 activation. We suggest that CDEE may be therapeutic for treating inflammatory diseases.
