Ginsenosides compound K and Rh2 inhibit tumor necrosis factor-α-induced activation of the NF-κB and JNK pathways in human astroglial cells

被引:128
作者
Choi, Kyungsun
Kim, Myungsun
Ryu, Jeonghee
Choi, Chulhee
机构
[1] Korea Adv Inst Sci & Technol, Dept Brain & Bioengn, Lab Computat Cell Biol, Taejon 305701, South Korea
[2] Korea Adv Inst Sci & Technol, Grad Sch Med Sci & Engn, Taejon 305701, South Korea
[3] Korea Adv Inst Sci & Technol, Inst Biocent, Taejon 305701, South Korea
关键词
glia; inflammation; ginsenosides; NF-kappa B; JNK; tumor necrosis factor;
D O I
10.1016/j.neulet.2007.05.017
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Ginsenosides, the main component of Panax ginseng, have been known for the anti-inflammatory and anti-proliferative activities. In this study, we investigated the molecular mechanisms responsible for the anti-inflammatory effects of ginsenosides on activated astroglial cells. Among 13 different ginsenosides. intestinal bacterial metabolites Rh and compound K (C-K) showed a significant inhibitory effect on tumor necrosis factor-alpha (TNF-alpha)-induced expression of intercellular adhesion molecule-1 in human astroglial cells. Pretreatment with C-K or Rh-2 suppressed TNF-alpha-induced phosphorylation Of I kappa B alpha. kinase and the subsequent phosphorylation and degradation Of I kappa B alpha. Additionally, the same treatment inhibited TNF-alpha-induced phosphorylation of MKK4 and the subsequent activation of the JNK-AP-1 pathway. The inhibitory effect of ginsenosides on TNF-alpha-induced activation of the NF-kappa B and JNK pathways was not observed in human monocytic U937 cells. These results collectively indicate that ginsenoside metabolites C-K and Rh-2 exert anti-inflammatory effects by the inhibition of both NF-kappa B and JNK pathways in a cell-specific manner. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:37 / 41
页数:5
相关论文
共 26 条
  • [1] Akao T, 1998, BIOL PHARM BULL, V21, P245, DOI 10.1248/bpb.21.245
  • [2] Ginsenosides Rg3 and Rh2 inhibit the activation of AP-1 and protein kinase A pathway in lipopolysaccharide/interferon-γ-stimulated BV-2 microqlial cells
    Bae, Eun-Ah
    Kim, Eun-Jin
    Park, Jin-Sun
    Kim, Hee-Sun
    Ryu, Jong Hoon
    Kim, Dong-Hyun
    [J]. PLANTA MEDICA, 2006, 72 (07) : 627 - 633
  • [3] Ginsenoside Rg1 reduces MPTP-induced substantia nigra neuron loss by suppressing oxidative stress
    Chen, XC
    Zhou, YC
    Chen, Y
    Zhu, YG
    Fang, F
    Chen, LM
    [J]. ACTA PHARMACOLOGICA SINICA, 2005, 26 (01) : 56 - 62
  • [4] Compare FDG-PET and Tc-99m tetrofosmin SPECT to detect metastatic thyroid carcinoma
    Chen, YK
    Liu, FY
    Yen, RF
    Kao, CH
    [J]. ACADEMIC RADIOLOGY, 2003, 10 (08) : 835 - 839
  • [5] Choi C, 1999, J IMMUNOL, V162, P1889
  • [6] Tumor necrosis factor-related apoptosis-inducing ligand induces caspase-dependent interleukin-8 expression and apoptosis in human astroglioma cells
    Choi, C
    Kutsch, O
    Park, J
    Zhou, T
    Seol, DW
    Benveniste, EN
    [J]. MOLECULAR AND CELLULAR BIOLOGY, 2002, 22 (03) : 724 - 736
  • [7] Induction of intercellular adhesion molecule-1 by Fas ligation: proinflammatory roles of Fas in human astroglioma cells
    Choi, K
    Benveniste, EN
    Choi, C
    [J]. NEUROSCIENCE LETTERS, 2003, 352 (01) : 21 - 24
  • [8] Effect of 17-β-estradiol and ginsenoside Rg1 on reactive microglia induced by β-amyloid peptides
    Gong, YS
    Zhang, JT
    [J]. JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH, 1999, 1 (03) : 153 - 161
  • [9] 3 NF-KAPPA-B SITES IN THE I-KAPPA-B-ALPHA PROMOTER ARE REQUIRED FOR INDUCTION OF GENE-EXPRESSION BY TNF-ALPHA
    ITO, CY
    KAZANTSEV, AG
    BALDWIN, AS
    [J]. NUCLEIC ACIDS RESEARCH, 1994, 22 (18) : 3787 - 3792
  • [10] Ginseng saponin metabolite suppresses phorbol ester-induced matrix metalloproteinase-9 expression through inhibition of activator protein-1 and mitogen-activated protein kinase signaling pathways in human astroglioma cells
    Jung, SH
    Woo, MS
    Kim, SY
    Kim, WK
    Hyun, JW
    Kim, EJ
    Kim, DH
    Kim, HS
    [J]. INTERNATIONAL JOURNAL OF CANCER, 2006, 118 (02) : 490 - 497