Upregulation of heme oxygenase-1 by ginsenoside Ro attenuates lipopolysaccharide-induced inflammation in macrophage cells

The beneficial effects of ginsenoside species have been well demonstrated in a number of studies. However, the function of ginsenoside Ro (GRo), an oleanane-type saponin, has not been sufficiently investigated. Thus, the aim of the present study was to investigate the anti-inflammatory effects of GR...

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Veröffentlicht in:Journal of ginseng research 2015, 39(4), , pp.365-370
Hauptverfasser: Kim, Sokho, Oh, Myung-Hoon, Kim, Bum-Seok, Kim, Won-Il, Cho, Ho-Seong, Park, Byoung-Yong, Park, Chul, Shin, Gee-Wook, Kwon, Jungkee
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Sprache:eng
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Zusammenfassung:The beneficial effects of ginsenoside species have been well demonstrated in a number of studies. However, the function of ginsenoside Ro (GRo), an oleanane-type saponin, has not been sufficiently investigated. Thus, the aim of the present study was to investigate the anti-inflammatory effects of GRo in vitro using the Raw 264.7 mouse macrophage cell line treated with lipopolysaccharide (LPS), and to clarify the possible mechanism of GRo involving heme oxygenase-1 (HO-1), which itself plays a critical role in self-defense in the presence of inflammatory stress. Raw 264.7 cells were pretreated with GRo (up to 200μM) for 1 h before treatment with 1 μg/mL LPS, and both cell viability and inflammatory markers involving HO-1 were evaluated. GRo significantly increased cell viability in a dose dependent manner following treatment with LPS, and decreased levels of reactive oxygen species and nitric oxide. GRo decreased inflammatory cytokines such as nitric oxide synthase and cyclooxygenase-2 induced by LPS. Moreover, GRo increased the expression of HO-1 in a dose dependent manner. Cotreatment of GRo with tin protoporphyrin IX, a selective inhibitor of HO-1, not only inhibited upregulation of HO-1 induced by GRo, but also reversed the anti-inflammatory effect of GRo in LPS treated Raw 264.7 cells. GRo induces anti-inflammatory effects following treatment with LPS via upregulation of HO-1.
ISSN:1226-8453
2093-4947
DOI:10.1016/j.jgr.2015.03.008