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Research ArticleNeuropharmacology

Anti-Inflammatory Mechanism of Compound K in Activated Microglia and Its Neuroprotective Effect on Experimental Stroke in Mice

Jin-Sun Park, Jin A. Shin, Ji-Sun Jung, Jin-Won Hyun, Thi Kim Van Le, Dong-Hyun Kim, Eun-Mi Park and Hee-Sun Kim
Journal of Pharmacology and Experimental Therapeutics April 2012, 341 (1) 59-67; DOI: https://doi.org/10.1124/jpet.111.189035
Jin-Sun Park
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Jin A. Shin
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Ji-Sun Jung
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Jin-Won Hyun
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Thi Kim Van Le
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Dong-Hyun Kim
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Eun-Mi Park
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Hee-Sun Kim
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Abstract

Microglial activation plays a pivotal role in the pathogenesis of various neurologic disorders, such as cerebral ischemia, Alzheimer's disease, and Parkinson's disease. Thus, controlling microglial activation is a promising therapeutic strategy for such brain diseases. In the present study, we found that a ginseng saponin metabolite, compound K [20-O-d-glucopyranosyl-20(S)-protopanaxadiol], inhibited the expressions of inducible nitric-oxide synthase, proinflammatory cytokines, monocyte chemotactic protein-1, matrix metalloproteinase-3, and matrix metalloproteinase-9 in lipopolysaccharide (LPS)-stimulated BV2 microglial cells and primary cultured microglia. Subsequent mechanistic studies revealed that compound K suppressed microglial activation via inhibiting reactive oxygen species, mitogen-activated protein kinases, and nuclear factor-κB/activator protein-1 activities with enhancement of heme oxygenase-1/antioxidant response element signaling. To address the anti-inflammatory effects of compound K in vivo, we used two brain disease models of mice: sepsis (systemic inflammation) and cerebral ischemia. Compound K reduced the number of Iba1-positive activated microglia and inhibited the expressions of tumor necrosis factor-α and interleukin-1β in the LPS-induced sepsis brain. Furthermore, compound K reduced the infarct volume of ischemic brain induced by middle cerebral artery occlusion and suppressed microglial activation in the ischemic cortex. The results collectively suggest that compound K is a promising agent for prevention and/or treatment of cerebral ischemia and other neuroinflammatory disorders.

Footnotes

  • This work was supported by the National Research Foundation of Korea, which is funded by the Korean government [Grant 2010-0029354].

  • Article, publication date, and citation information can be found at http://jpet.aspetjournals.org.

    http://dx.doi.org/10.1124/jpet.111.189035.

  • ABBREVIATIONS:

    ROS
    reactive oxygen species
    AP-1
    activator protein-1
    ARE
    antioxidant response element
    CBF
    cerebral blood flow
    CRE
    cAMP responsive element
    CREB
    CRE-binding protein
    E2
    enhancer 2
    EMSA
    electrophoretic mobility-shift assay
    GR
    glucocorticoid receptor
    HO-1
    heme oxygenase-1
    IL-6
    interleukin-6
    NO
    nitric oxide
    iNOS
    inducible NO synthase
    LPS
    lipopolysaccharide
    MAPK
    mitogen-activated protein kinase
    MCAO
    middle cerebral artery occlusion
    MCP
    monocyte chemotactic protein-1
    MMP
    matrix metalloproteinase
    NF-κB
    nuclear factor-κB
    TBST
    10 mM Tris-HCl containing 150 mM NaCl and 0.5% Tween 20
    TNF
    tumor necrosis factor
    RT-PCR
    reverse transcription-polymerase chain reaction.

  • Received October 13, 2011.
  • Accepted December 28, 2011.
  • Copyright © 2012 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 341 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 341, Issue 1
1 Apr 2012
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Research ArticleNeuropharmacology

Anti-Inflammatory and Neuroprotective Effects of Compound K

Jin-Sun Park, Jin A. Shin, Ji-Sun Jung, Jin-Won Hyun, Thi Kim Van Le, Dong-Hyun Kim, Eun-Mi Park and Hee-Sun Kim
Journal of Pharmacology and Experimental Therapeutics April 1, 2012, 341 (1) 59-67; DOI: https://doi.org/10.1124/jpet.111.189035

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Research ArticleNeuropharmacology

Anti-Inflammatory and Neuroprotective Effects of Compound K

Jin-Sun Park, Jin A. Shin, Ji-Sun Jung, Jin-Won Hyun, Thi Kim Van Le, Dong-Hyun Kim, Eun-Mi Park and Hee-Sun Kim
Journal of Pharmacology and Experimental Therapeutics April 1, 2012, 341 (1) 59-67; DOI: https://doi.org/10.1124/jpet.111.189035
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