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논문 기본 정보

자료유형
학술저널
저자정보
Saeromi Kang (Pusan National University) Soo-Jin Park (Pusan National University) Ae-Yeon Lee (Pusan National University) Jin Huang (Pusan National University) Hae-Young Chung (Pusan National University) Dong-Soon Im (Pusan National University)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.42 No.1
발행연도
2018.1
수록면
68 - 74 (7page)

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초록· 키워드

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Background: Ginsenosides have been reported to have many health benefits, including antiinflammatory effects, and the resolution of inflammation is now considered to be an active process driven by M2-type macrophages. In order to determine whether ginsenosides modulate macrophage phenotypes to reduce inflammation, 11 ginsenosides were studied with respect to macrophage polarization and the resolution of inflammation.
Methods: Mouse peritoneal macrophages were polarized into M1 or M2 phenotypes. Reverse transcription-polymerase chain reaction, Western blotting, and measurement of nitric oxide (NO) and prostaglandin E2 levels were performed in vitro and in a zymosan-induced peritonitis C57BL/6 mouse model.
Results: Ginsenoside Rg₃ was identified as a proresolving ginseng compound based on the induction of M2 macrophage polarization. Ginsenoside Rg₃ not only induced the expression of arginase-1 (a representative M2 marker gene), but also suppressed M1 marker genes, such as inducible NO synthase, and NO levels. The proresolving activity of ginsenoside Rg₃ was also observed in vivo in a zymosan-induced peritonitis model. Ginsenoside Rg₃ accelerated the resolution process when administered at peak inflammatory response into the peritoneal cavity.
Conclusion: These results suggest that ginsenoside Rg₃ induces the M2 polarization of macrophages and accelerates the resolution of inflammation. This finding opens a new avenue in ginseng pharmacology.

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ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References

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UCI(KEPA) : I410-ECN-0101-2018-524-001744567