Ginsenosides compound K and Rh2 inhibit tumor necrosis factor-α-induced activation of the NF-κB and JNK pathways in human astroglial cells
Ginsenosides compound K and Rh2 inhibit tumor necrosis factor-α-induced activation of the NF-κB and JNK pathways in human astroglial cells
复制标题
DOI：
10.1016/j.neulet.2007.05.017
复制
发表时间：
2007-06-21
影响因子：
2.5
通讯作者：
Choi, Chulhee
中科院分区：
文献类型：
--
作者：
Choi, Kyungsun;Kim, Myungsun;Choi, Chulhee
人参皂苷是人参的主要成分，具有抗炎和抗增殖活性。在这项研究中，我们调查的分子机制，负责对激活的星形胶质细胞的抗炎作用的皂苷。在13种不同的皂苷中。肠细菌代谢物Rh和化合物K（C-K）对肿瘤坏死因子-α（TNF-α）诱导的人星形胶质细胞中细胞间粘附分子-1的表达显示出显著的抑制作用。用C-K或Rh-2预处理抑制TNF-α诱导的I κ B α磷酸化。激酶以及随后的I κ B α的磷酸化和降解。此外，相同的处理抑制TNF-α诱导的MKK 4磷酸化和随后的JNK-AP-1通路活化。在人单核细胞U937细胞中未观察到黄芪皂苷对TNF-α诱导的NF-κ B和JNK通路活化的抑制作用。这些结果共同表明，TNF-α代谢物C-K和Rh-2通过以细胞特异性方式抑制NF-κ B和JNK途径发挥抗炎作用。(c)2007爱思唯尔爱尔兰有限公司保留所有权利。
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.