2. Academic Validation
  3. Upregulation of heme oxygenase-1 by ginsenoside Ro attenuates lipopolysaccharide-induced inflammation in macrophage cells

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

  • J Ginseng Res. 2015 Oct;39(4):365-70. doi: 10.1016/j.jgr.2015.03.008.
Sokho Kim 1,  Myung-Hoon Oh 1,  Bum-Seok Kim 2,  Won-Il Kim 2,  Ho-Seong Cho 2,  Byoung-Yong Park 2,  Chul Park 2,  Gee-Wook Shin 2,  Jungkee Kwon 3
Affiliations

Affiliations

  • 1 Department of Laboratory Animal Medicine, Chonbuk National University, Jetonju, Korea.
  • 2 Bio-safety Institute, College of Veterinary Medicine, Chonbuk National University, Jeonju, Korea.
  • 3 Department of Laboratory Animal Medicine, Chonbuk National University, Jetonju, Korea; Bio-safety Institute, College of Veterinary Medicine, Chonbuk National University, Jeonju, Korea.
PMID: 26869829 DOI: 10.1016/j.jgr.2015.03.008
Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusion: GRo induces anti-inflammatory effects following treatment with LPS via upregulation of HO-1.

Keywords

ginsenoside Ro; heme oxygenase-1; inflammation; lipopolysaccharide; macrophage.

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