Effects of Root Extracts from Angelica gigas and Angelica acutiloba on Inflammatory Mediators in Mouse Macrophages

  • Yoon, Tae-Sook (Department of Herbal Resources Research, Korea Institute of Oriental Medicine) ;
  • Cheon, Myeoung-Sook (Department of Herbal Resources Research, Korea Institute of Oriental Medicine) ;
  • Lee, Do-Yeon (Department of Herbal Resources Research, Korea Institute of Oriental Medicine) ;
  • Moon, Byeong-Cheol (Department of Herbal Resources Research, Korea Institute of Oriental Medicine) ;
  • Lee, Hye-Won (Department of Herbal Resources Research, Korea Institute of Oriental Medicine) ;
  • Choo, Byung-Kil (Department of Herbal Resources Research, Korea Institute of Oriental Medicine) ;
  • Kim, Ho-Kyoung (Department of Herbal Resources Research, Korea Institute of Oriental Medicine)
  • Published : 2007.12.31

Abstract

Root extracts of Angelica gigas and A. acutiloba have been used traditionally for the treatment of gynecological diseases, as well as anemia, blood stasis, and inflammatory pain, as blood tonics in Oriental medicine. In the present study, we investigated the effects of A. gigas and A. acutiloba on inflammatory mediators in mouse macrophages and compared their activities. Many studies suggest that prostaglandin $E_2$ ($PGE_2$) biosynthesis and nitric oxide (NO) production play important roles in the processes of both inflammation and carcinogenesis. Ethanolic extracts from the roots of both species exhibited significant inhibitory effects on $PGE_2$ generation in lipopolysaccharide-stimulated RAW 264.7 cells. In particular, the extract from A. gigas was more effective than that from A. acutiloba. Although neither inhibited NO generation, the extract from A. acutiloba stimulated NO generation. Our results suggest that the roots of A. gigas might possess more anti-inflammatory and/or cancer chemopreventative activity than that of A. acutiloba due to the suppression of cyclooxygenase-2 (COX2)-mediated $PGE_2$ production. In addition, A. acutiloba might exert anti-tumor activity through an increase in macrophage-produced NO.

Keywords

References

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