TY - JOUR
T1 - Inhibition of TLR ligand- and interferon gamma-induced murine microglial activation by Panax notoginseng
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
Y1 - 2012/6
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
UR - http://www.scopus.com/inward/record.url?scp=84866514986&partnerID=8YFLogxK
U2 - 10.1007/s11481-011-9333-0
DO - 10.1007/s11481-011-9333-0
M3 - Article
C2 - 22183805
AN - SCOPUS:84866514986
SN - 1557-1890
VL - 7
SP - 465
EP - 476
JO - Journal of NeuroImmune Pharmacology
JF - Journal of NeuroImmune Pharmacology
IS - 2
ER -