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KMID : 0861020130280060145
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Korea Journal of Herbology
2013 Volume.28 No. 6 p.145 ~ p.153
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Ginsenoside Rg1 Attenuates Neuroinflammation Following Systemic Lipopolysaccharide Treatment in Mice
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Shin Jung-Won
Ma Sun-Ho
Lee Ju-Won
Kim Dong-Kyu
Do Kyu-Ho
Sohn Nak-Won
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Abstract
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Objectives: Neuroinflammation is characterized by microglial activation and the expression of major inflammatory mediators. The present study investigated the inhibitory effect of ginsenoside Rg1 (GRg1), a principle active ingredient in Panax ginseng, on pro-inflammatory cytokines and microglial activation induced by systemic lipopolysaccharide (LPS) treatment in the mouse brain tissue.
Methods : Varying doses of GRg1 was orally administered (10, 20, and 30 mg/kg) 1 h before the LPS injection (3 mg/kg, intraperitoneally). The mRNA expression of pro-inflammatory cytokines in the brain tissue was measured using the quantitative real-time PCR method at 4 h after the LPS injection, Microglial activation was evaluated using western blotting and immunohistochemistry against ionized calcium binding adaptor molecule 1 (Iba1) in the brain tissue. Cyclooxigenase-2 (COX-2) expressions also observed using western blotting and immunohistochemistry at 4 h after the LPS injection, In addition, double-immunofluorescent labeling of tumor necrosis factor-α (TNF-α) and COX-2 with microglia and neurons was processed in the brain tissue.
Results : GRg1 (30 mg/kg) significantly attenuated the upregulation of TNF-α, interleukin (IL)-1β and IL-6 mRNA in the brain tissue at 4 h after LPS injection. Morphological activation and Iba1 protein expression of microglia induced by systemic LPS injection were reduced by the GRg1 (30 mg/kg) treatment. Upregulation of COX-2 protein expression in the brain tissue was also attenuated by the GRg1 (30 mg/kg) treatment.
Conclusion : The results suggest that GRg1 is effective in the early stage of neuroinflammation which causes neurodegenerative diseases.
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KEYWORD
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Ginsenoside Rg1, Neuroinflammation, Pro-inflammatory Cytokines, Microglia activation, Cyclooxygense-2
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