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자료유형
학술저널
저자정보
Chun, Jin-Mi (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Cheon, Myeong-Sook (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Park, Mi-Kyung (Laboratory of Chemical Genomics, Pharmacology Research Center, Korea Research Institute of Chemical Technology) Lee, A-Yeong (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Moon, Byeong-Cheol (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Ji, Yun-Ui (Center of Herbal Resources Research, Korea Institute of Oriental Medicine) Kim, Ho-Kyoung (Center of Herbal Resources Research, Korea Institute of Oriental Medicine)
저널정보
한국응용생명화학회 Applied Biological Chemistry Applied Biological Chemistry 제55권 제1호
발행연도
2012.1
수록면
41 - 46 (6page)

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Cephalonoplos segetum has been used as an herbal remedy, and is considered to have anti-inflammatory potential. However, its biological mechanism in this treatment process remains unknown. Therefore, the anti-inflammatory activity of the ethyl acetate fraction of C. segetum extracts (CSE-EA), more active than C. segetum extracts (CSE) in murine macrophages, was investigated. Production levels of nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), and interleukin-$1{\beta}$ (IL-$1{\beta}$) by lipopolysaccharide (LPS)-induced RAW 264.7 macrophages were measured by ELISA. In addition, protein expression levels of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2, and the phosphorylation of mitogen-activated protein kinases (MAPKs) in the LPS-induced macrophages were investigated by Western blotting. The CSE-EA (50, 100 or 200 ${\mu}g/mL$) significantly inhibited NO, $PGE_2$, TNF-${\alpha}$, and IL-$1{\beta}$ production in LPS-induced macrophages in a dose-dependent manner with 50% inhibitory concentration values of 80.4, 104.7, 91.3, and 46.7 ${\mu}g/mL$, respectively. Similarly, CSE-EA reduced protein expression of iNOS and COX-2 and led to the attenuated activation of kinases ERK1/2 and JNK in the macrophages. Results of the present study suggest that the anti-inflammatory effects of CSE-EA are likely due to the down-regulation of NO, $PGE_2$ TNF-${\alpha}$, and IL-$1{\beta}$ and the reduced expression of iNOS and COX-2 via suppression of MAPK signaling pathways in LPS-induced murine macrophages.

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