Chloroform Fraction of Zingiberis Rhizoma Recens Modulates the Production of Inflammatory Mediators in LPS-stimulated BV2 Microglial Cells

생강 클로로포름 분획의 활성화된 뇌신경교세포(腦神經膠細胞)에서 염증반응 억제효과

  • Seo, Un-Kyo (Department of Internal Medicine, Dongguk University Bundang Oriental Hospital) ;
  • Jung, Hyo-Won (Department of Herbology, College of Oriental Medicine Dongguk University) ;
  • Park, Yong-Ki (Department of Herbology, College of Oriental Medicine Dongguk University, Oriental Medicine Drug R&D Center, College of Oriental Medicine, Dongguk University)
  • 서운교 (동국대학교 분당한방병원 내과) ;
  • 정효원 (동국대학교 한의과대학 본초학교실) ;
  • 박용기 (동국대학교 한의과대학 본초학교실, 동국대학교 한의과대학 한방신약개발센터)
  • Published : 2008.09.30

Abstract

Objectives : The root of Zingiber officinale ROSC. (Zingiberis Rhizoma Recens; Ginger) has been widely used as one of folk remedies and food materials in many traditional preparations. Ginger is known as an effective appetite enhancer and anti-inflammatory agent. This study was performed to investigate the effect of ginger chloroform fraction (GCF) in microglia which play a central role on brain inflammation in neurodegenerative diseases. Methods : Dried ginger was extracted with 80% methanol, and then fractionated with chloroform. BV2 mouse microglial cells were cultured with different concentrations of GCF and then stimulated with LPS (1 ${\mu}g/m{\ell}$) at indicated times. The cell toxicity of GCF was determined by MTT assay. The concentrations of NO, PGE2 and cytokines were measured by Griess assay and enzyme-linked immunosorbant assay. The mRNA and protein expressions of iNOS, COX-2 and cytokines were determined by RT-PCR and Western blotting. The phosphorylation of three MAPKs (p38 MAPK, ERK1/2 and JNK) and $NF-{\kappa}B$ activation were determined by Western blotting. Results : GCF significantly inhibited LPS-induced production of inflammatory mediators, NO, $PGE_2$ and proinflammatory cytokines ($TNF-{\alpha}$ and $IL-1{\beta}$) in a dose-dependent manner. GCF attenuated LPS-induced expression of mRNA and protein of inflammatory enzymes, iNOS, COX-2 and proinflammatory cytokines through suppressing the phosphorylation of ERK1/2 and p38 MAPK and the activation of p65 $NF-{\kappa}B$ in BV2 cells. Conclusions : This study suggests that GCF may have an anti-inflammatory property through suppressing the inflammatory mediator production released by activated microglia after the brain injury.

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