›› 2012, Vol. 43 ›› Issue (1): 13-18.doi: 10.3969/j.issn.0529-1356.2012.01.003

• 神经生物学 • 上一篇    下一篇

三七皂苷Rg1抑制脂多糖诱导的小胶质细胞激活

宗一1; 戴纪男1; 孙俊1; 杨萍1; 张伟2; 艾青龙2* ; 陆地1*   

  1. 1.昆明医学院人体解剖学教研室,昆明650500; 2.昆明医学院第一附属医院神经内科,昆明650011
  • 收稿日期:2011-05-16 修回日期:2011-07-06 出版日期:2012-02-06
  • 通讯作者: 艾青龙; 陆地

Ginsenoside Rg1 inhibiting the lipopolysaccharide-induced activation of microglial cells

  1. 1.Department of Anatomy, Kunming Medical University, Kunming 650500, China; 2.Department of Neurology, the First Affiliated Hospital of Kunming Medical University, Kunming 650011,China
  • Received:2011-05-16 Revised:2011-07-06 Online:2012-02-06
  • Contact: 艾青龙; 陆地

关键词: 三七皂苷Rg1, 脂多糖, 炎性因子, 反转录-聚合酶链式反应, 免疫荧光, BV-2细胞

Abstract: Objective To investigate whether ginsenoside Rg1 (Rg1) inhibits the expression of potentially pro-inflammatory cytokines by cultured murine microglial BV-2 cells stimulated with lipopolysaccharide (LPS). Methods An inflammatory cell model was structured by LPS-stimulated microglial BV-2 cells. The inflammatory cells were treated with Rg1 (10,20 and 40μmol/L) prior to LPS exposure. The effects on the mRNA and protein levels of pro-inflammatory enzymes, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and inflammatory signaling proteins nuclear factor-κB (NF-κB) were analysed by reverse transcription -polymerase chain reaction (RT-PCR) and immunofluorescence staining assay. The effects of Rg1 on viability of BV-2 cells were measured by MTT assay. Results The results indicated that LPS-induced iNOS and COX-2 protein and mRNA expression levels decreased significantly by Rg1 in a concentration-dependent manner. Rg1 also had an effect on the expression of TNF-α, IL-1β and NF-κB through transcriptional and translational inhibition. In addition, Rg1 dose-dependently decreased the increasing expression

Key words: Ginsenoside Rg1, Lipopolysaccharide, Pro-inflammatory cytokine, RT-PCR, Immunofluorescence, BV-2 cell

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