| Autor: |
Saeromi Kang, Soo-Jin Park, Ae-Yeon Lee, Jin Huang, Hae-Young Chung, Dong-Soon Im |
| Jazyk: |
angličtina |
| Rok vydání: |
2018 |
| Předmět: |
|
| Zdroj: |
Journal of Ginseng Research, Vol 42, Iss 1, Pp 68-74 (2018) |
| Druh dokumentu: |
article |
| ISSN: |
1226-8453 |
| DOI: |
10.1016/j.jgr.2016.12.012 |
| Popis: |
Background: Ginsenosides have been reported to have many health benefits, including anti-inflammatory 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. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
|
