title: Anti-Inflammatory Effects of Ginsenoside-Rh2 Inhibits LPS-Induced Activation of Microglia and Overproduction of Inflammatory Mediators Via Modulation of TGF-β1/Smad Pathway.
abstract: Microglia activation plays an important role in neuroinflammation and contributes to several neurological disorders. Hence, inhibition of both microglia activation and pro-inflammatory cytokines may lead to the effective treatment of neurodegenerative diseases. In this study, we found that GRh2 inhibited the inflammatory response to lipopolysaccharide (LPS) and prevented the LPS-induced neurotoxicity in microglia cells. GRh2 significantly decreased the generation of nitric oxide production, and tumor necrosis factor-α, interleukin (IL)-6, IL-1β, cyclooxygenase-2 and inducible nitric oxide synthase in LPS-induced activated microglia cells. Furthermore, GRh2 (20 and 50 μM) significantly increased TGF-β1 expression and reduced the expression of Smad. These results suggest that GRh2 effectively inhibits microglia activation and production of pro-inflammatory cytokines via modulating the TGF-β1/Smad pathway.
authors.affiliation: Department of Herbology, College of Korean Medicine, Dongguk University, Gyeongju, 780-714, Republic of Korea.
authors.forename: R
authors.initials: R
authors.lastname: Vinoth Kumar
authors.affiliation: Korean Medicine R&D Center, Dongguk University, Gyeongju, 780-714, Republic of Korea.
authors.forename: Tae Woo
authors.initials: TW
authors.lastname: Oh
authors.affiliation: Department of Herbology, College of Korean Medicine, Dongguk University, Gyeongju, 780-714, Republic of Korea. yongki@dongguk.ac.kr.|Korean Medicine R&D Center, Dongguk University, Gyeongju, 780-714, Republic of Korea. yongki@dongguk.ac.kr.
authors.forename: Yong-Ki
authors.initials: YK
authors.lastname: Park
mesh_terms: D000818:Animals; D002460:Cell Line; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D036145:Ginsenosides / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000378:metabolism*; D053583:Interleukin-1beta / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000494:pharmacology*; D051379:Mice; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009569:Nitric Oxide / Q000096:biosynthesis; D019001:Nitric Oxide Synthase / Q000096:biosynthesis; D015398:Signal Transduction; D051785:Smad Proteins / Q000378:metabolism*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D036145:Ginsenosides; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D018696:Neuroprotective Agents; D051785:Smad Proteins; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; C055305:ginsenoside Rh2; D019001:Nitric Oxide Synthase; D051546:Cyclooxygenase 2
keywords: BV-2 microglia cells; GRh2; Lipopolysaccharide; TGF-β1/Smad