Inhibition of TLR ligand- and interferon gamma-induced murine microglial activation by Panax notoginseng

Celine A. Beamer; David M. Shepherd

doi:10.1007/s11481-011-9333-0

Inhibition of TLR ligand- and interferon gamma-induced murine microglial activation by Panax notoginseng

Celine A. Beamer
, David M. Shepherd

Research output: Contribution to journal › Article › peer-review

25 Scopus citations

Abstract

Among the many products which influence microglial activation and resulting neuroinflammation, herbal medicine has recently drawn much attention due to its immunomodulatory and neuroprotective activities. The purpose of the current study was to investigate the effects of an extract of Panax notoginseng (NotoG™) on TLR ligandand IFNγ-induced activation in N9 and EOC20 microglial cells lines. NotoG suppressed microglial activation as measured by reduced expression of accessory molecules (CD40 and CD86), decreased production of inflammatory mediators (IL-6 and TNFα), and diminished release of antibacterial products (nitric oxide). Furthermore, this immunosuppressive activity was neither dependent on the glucocorticoid receptor, nor the result of a single ginsenosides (Rb1, Rg1, or Re), which are the major active constituents of the whole extract. NotoG and select ginsenosides may therefore be of therapeutic benefit in treating or preventing neurodegenerative diseases such as multiple sclerosis and parkinson's disease.

Original language	English
Pages (from-to)	465-476
Number of pages	12
Journal	Journal of NeuroImmune Pharmacology
Volume	7
Issue number	2
DOIs	https://doi.org/10.1007/s11481-011-9333-0
State	Published - Jun 2012

Funding

Acknowledgments This work is supported by NIH grants COBRE P20 RR17670 from the National Center for Research Resources (NCRR) and NRSA fellowship ES-013044 (CAB). The authors wish to thank Pamela Shaw and the CEHS Fluorescence Core, as well as Dr. Darrell Jackson at UM for their expert technical assistance.

Funder number
COBRE P20 RR17670
F32ES013044
ES-013044

Keywords

Cytokine
Ginsenoside
Glucocorticoid receptor
Inflammation
Nitric oxide

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10.1007/s11481-011-9333-0

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title = "Inhibition of TLR ligand- and interferon gamma-induced murine microglial activation by Panax notoginseng",

abstract = "Among the many products which influence microglial activation and resulting neuroinflammation, herbal medicine has recently drawn much attention due to its immunomodulatory and neuroprotective activities. The purpose of the current study was to investigate the effects of an extract of Panax notoginseng (NotoG{\texttrademark}) on TLR ligandand IFNγ-induced activation in N9 and EOC20 microglial cells lines. NotoG suppressed microglial activation as measured by reduced expression of accessory molecules (CD40 and CD86), decreased production of inflammatory mediators (IL-6 and TNFα), and diminished release of antibacterial products (nitric oxide). Furthermore, this immunosuppressive activity was neither dependent on the glucocorticoid receptor, nor the result of a single ginsenosides (Rb1, Rg1, or Re), which are the major active constituents of the whole extract. NotoG and select ginsenosides may therefore be of therapeutic benefit in treating or preventing neurodegenerative diseases such as multiple sclerosis and parkinson's disease.",

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author = "Beamer, \{Celine A.\} and Shepherd, \{David M.\}",

note = "Funding Information: Acknowledgments This work is supported by NIH grants COBRE P20 RR17670 from the National Center for Research Resources (NCRR) and NRSA fellowship ES-013044 (CAB). The authors wish to thank Pamela Shaw and the CEHS Fluorescence Core, as well as Dr. Darrell Jackson at UM for their expert technical assistance.",

year = "2012",

month = jun,

doi = "10.1007/s11481-011-9333-0",

language = "English",

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AU - Beamer, Celine A.

AU - Shepherd, David M.

N1 - Funding Information: Acknowledgments This work is supported by NIH grants COBRE P20 RR17670 from the National Center for Research Resources (NCRR) and NRSA fellowship ES-013044 (CAB). The authors wish to thank Pamela Shaw and the CEHS Fluorescence Core, as well as Dr. Darrell Jackson at UM for their expert technical assistance.

PY - 2012/6

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N2 - Among the many products which influence microglial activation and resulting neuroinflammation, herbal medicine has recently drawn much attention due to its immunomodulatory and neuroprotective activities. The purpose of the current study was to investigate the effects of an extract of Panax notoginseng (NotoG™) on TLR ligandand IFNγ-induced activation in N9 and EOC20 microglial cells lines. NotoG suppressed microglial activation as measured by reduced expression of accessory molecules (CD40 and CD86), decreased production of inflammatory mediators (IL-6 and TNFα), and diminished release of antibacterial products (nitric oxide). Furthermore, this immunosuppressive activity was neither dependent on the glucocorticoid receptor, nor the result of a single ginsenosides (Rb1, Rg1, or Re), which are the major active constituents of the whole extract. NotoG and select ginsenosides may therefore be of therapeutic benefit in treating or preventing neurodegenerative diseases such as multiple sclerosis and parkinson's disease.

AB - Among the many products which influence microglial activation and resulting neuroinflammation, herbal medicine has recently drawn much attention due to its immunomodulatory and neuroprotective activities. The purpose of the current study was to investigate the effects of an extract of Panax notoginseng (NotoG™) on TLR ligandand IFNγ-induced activation in N9 and EOC20 microglial cells lines. NotoG suppressed microglial activation as measured by reduced expression of accessory molecules (CD40 and CD86), decreased production of inflammatory mediators (IL-6 and TNFα), and diminished release of antibacterial products (nitric oxide). Furthermore, this immunosuppressive activity was neither dependent on the glucocorticoid receptor, nor the result of a single ginsenosides (Rb1, Rg1, or Re), which are the major active constituents of the whole extract. NotoG and select ginsenosides may therefore be of therapeutic benefit in treating or preventing neurodegenerative diseases such as multiple sclerosis and parkinson's disease.

KW - Cytokine

KW - Ginsenoside

KW - Glucocorticoid receptor

KW - Inflammation

KW - Nitric oxide

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ER -

Inhibition of TLR ligand- and interferon gamma-induced murine microglial activation by Panax notoginseng

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Keywords

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