title: Ginsenoside Rg3 attenuates microglia activation following systemic lipopolysaccharide treatment in mice.
abstract: Neuroinflammation, characterized by activation of microglia and expression of major inflammatory mediators, contributes to neuronal damage in addition to acute and chronic central nervous system (CNS) disease progression. The present study investigated the immune modulatory effects of ginsenoside Rg3, a principle active ingredient in Panax ginseng, on pro-inflammatory cytokines and microglia activation in brain tissue induced by systemic lipopolysaccharide (LPS) treatment in C57BL/6 mice. Systemic LPS treatment induces immediate microglia activation in the brain. Based on this information, ginsenoside Rg3 was treated orally with 10, 20, and 30 mg/kg 1 h prior to the LPS (3 mg/kg, intraperitoneally (i.p.)) injection. Ginsenoside Rg3 at 20 and 30 mg/kg oral doses significantly attenuated up-regulation of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and IL-6 mRNA in brain tissue at 4 h after LPS injection. Morphological activation of microglia and Iba1 protein expression by systemic LPS injection were reduced with ginsenoside Rg3 (30 mg/kg) treatment. In addition, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in brain tissue were also attenuated with oral treatment of ginsenoside Rg3 at 30 mg/kg. These results indicate that ginsenoside Rg3 plays a modulatory role in neuroinflammation. This study shows that ginsenoside Rg3 attenuates microglia activation using an in vivo animal model.
authors.affiliation: Department of Oriental Medical Science, Graduate School of East-West Medical Science, Kyung Hee University, Yongin, South Korea.
authors.forename: Sun-Min
authors.initials: SM
authors.lastname: Park
authors.forename: Moon-Suk
authors.initials: MS
authors.lastname: Choi
authors.forename: Nak-Won
authors.initials: NW
authors.lastname: Sohn
authors.forename: Jung-Won
authors.initials: JW
authors.lastname: Shin
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D016207:Cytokines / Q000378:metabolism; D036145:Ginsenosides / Q000494:pharmacology / Q000627:therapeutic use*; D007155:Immunologic Factors / Q000494:pharmacology / Q000627:therapeutic use; D007249:Inflammation / Q000378:metabolism / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism*; D008070:Lipopolysaccharides; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D005894:Panax / Q000737:chemistry*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D012333:RNA, Messenger / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D052246:Cyclooxygenase 2 Inhibitors; D016207:Cytokines; D036145:Ginsenosides; D007155:Immunologic Factors; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D010936:Plant Extracts; D012333:RNA, Messenger; C097367:ginsenoside Rg3; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2