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Ginsenoside Rg1 Attenuates Lipopolysaccharide-Induced Inflammatory Responses Via the Phospholipase C-gamma 1 Signaling Pathway in Murine BV-2 Microglial Cells  期刊论文  

  • 编号:
    ef1ba7f1-a823-4a93-a721-09e41db3b390
  • 作者:
    Zong, Y.#[1]Ai, Q. L.(艾青龙)#[2]Zhong, L. M.[2];Dai, J. N.[1];Yang, P.[1];He, Y.[1];Sun, J.[1];Ling, E. A.*[1,3]Lu, D.(陆地)*[1,4]
  • 语种:
    英文
  • 期刊:
    CURRENT MEDICINAL CHEMISTRY ISSN:0929-8673 2012 年 19 卷 5 期 (770 - 779) ; FEB
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  • 摘要:

    Background and Purpose: Microglial activation plays an important role in neurodegenerative diseases by producing an array of proinflammatory enzymes and cytokines. Ginsenoside Rg1 (Rg1), a well-known Chinese herbal medicine, has been well recognized for its anti-inflammatory effect. This study sought to determine the anti-inflammatory effects of Rg1 and its underlying mechanisms in lipopolysaccharide (LPS)-stimulated murine BV-2 microglial cells.
    Experimental Approach: Murine BV-2 microglial cells were treated with Rg1 (10, 20, and 40 mu M) and/or LPS (1 mu g.ml(-1)). The mRNA and protein levels of proinflammatory proteins and cytokines were analysed by RT-PCR assay and double immunofluorescence labeling, respectively. Phosphorylation levels of mitogen-activated protein kinases (MAPKs) cascades, inhibitor kappa B-alpha (I kappa B-alpha) and cyclic AMP-responsive element (CRE)-binding protein (CREB) were measured by western blot. U73122 (5 mu M), a specific phospholipase C (PLC) inhibitor, was used to determine if PLC signaling pathway might be involved in Rg1's action on activated BV-2 cells.
    Key Results: Pretreatment with Rg1 significantly attenuated the LPS-induced expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and nuclear factor-kappa B (NF-kappa B) in BV-2 cells. U73122 blocked the effects of Rg1 on LPS-induced microglial activation. In addition, PLC-gamma 1 inhibition partially abolished the inhibitory effect of Rg1 on the phosphorylation of I kappa B-alpha, CREB, extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK).
    Conclusion and Implications: This investigation demonstrates that Rg1 significantly attenuates overactivation of microglial cells by repressing expression levels of neurotoxic proinflammatory mediators and cytokines via activation of PLC-gamma 1 signaling pathway.

  • 推荐引用方式
    GB/T 7714:
    Zong Y.,Ai Q. -L.,Zhong L. -M., et al. Ginsenoside Rg1 Attenuates Lipopolysaccharide-Induced Inflammatory Responses Via the Phospholipase C-gamma 1 Signaling Pathway in Murine BV-2 Microglial Cells [J].CURRENT MEDICINAL CHEMISTRY,2012,19(5):770-779.
  • APA:
    Zong Y.,Ai Q. -L.,Zhong L. -M.,Dai J. -N.,&Lu D..(2012).Ginsenoside Rg1 Attenuates Lipopolysaccharide-Induced Inflammatory Responses Via the Phospholipase C-gamma 1 Signaling Pathway in Murine BV-2 Microglial Cells .CURRENT MEDICINAL CHEMISTRY,19(5):770-779.
  • MLA:
    Zong Y., et al. "Ginsenoside Rg1 Attenuates Lipopolysaccharide-Induced Inflammatory Responses Via the Phospholipase C-gamma 1 Signaling Pathway in Murine BV-2 Microglial Cells" .CURRENT MEDICINAL CHEMISTRY 19,5(2012):770-779.
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