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生物活性导向鉴定及细胞信号技术用于阐明人参对人原单核细胞U937细胞的免疫调节作用。

Bioactivity-guided identification and cell signaling technology to delineate the immunomodulatory effects of Panax ginseng on human promonocytic U937 cells.

作者信息

Lee Davy C W, Yang Cindy L H, Chik Stanley C C, Li James C B, Rong Jian-hui, Chan Godfrey C F, Lau Allan S Y

机构信息

Cytokine Biology Group, Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region, PR China.

出版信息

J Transl Med. 2009 May 14;7:34. doi: 10.1186/1479-5876-7-34.

DOI:10.1186/1479-5876-7-34
PMID:19442267
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2689162/
Abstract

BACKGROUND

Ginseng is believed to have beneficial effects against human diseases, and its active components, ginsenosides, may play critical roles in its diverse physiological actions. However, the mechanisms underlying ginseng's effects remain to be investigated. We hypothesize some biological effects of ginseng are due to its anti-inflammatory effects.

METHODS

Human promonocytic U937 cells were used to investigate the immunomodulatory effects of ginseng following TNF-alpha treatment. A global gene expression profile was obtained by using genechip analysis, and specific cytokine expression was measured by quantitative RT-PCR and ELISA. HPLC was used to define the composition of ginsenosides in 70% ethanol-water extracts of ginseng. Activation of signalling kinases was examined by Western blot analysis.

RESULTS

Seventy percent ethanol-water extracts of ginseng significantly inhibited the transcription and secretion of CXCL-10 following TNF-alpha stimulation. Nine ginsenosides including Rb1, Rb2, Rc, Rd, Re, Rf, Rg1, Rg3 and Rh1 were identified in our extract by HPLC. Seven out of nine ginsenosides could significantly inhibit TNF-alpha-induced CXCL-10 expression in U937 cells and give comparable inhibition of CXCL-10 transcription to those with the extract. However, the CXCL-10 suppressive effect of individual ginsenosides was less than that of the crude extract or the mixture of ginsenosides. The CXCL-10 suppression can be correlated with the inactivation of ERK1/2 pathways by ginseng.

CONCLUSION

We showed ginseng suppressed part of the TNF-alpha-inducible cytokines and signalling proteins in promonocytic cells, suggesting that it exerts its anti-inflammatory property targeting at different levels of TNF-alpha activity. The anti-inflammatory role of ginseng may be due to the combined effects of ginsenosides, contributing in part to the diverse actions of ginseng in humans.

摘要

背景

人参被认为对人类疾病具有有益作用,其活性成分人参皂苷可能在其多种生理作用中发挥关键作用。然而,人参作用的潜在机制仍有待研究。我们推测人参的某些生物学效应归因于其抗炎作用。

方法

使用人原单核细胞U937细胞研究人参在肿瘤坏死因子-α(TNF-α)处理后的免疫调节作用。通过基因芯片分析获得全局基因表达谱,并通过定量逆转录聚合酶链反应(RT-PCR)和酶联免疫吸附测定(ELISA)测量特定细胞因子的表达。采用高效液相色谱法(HPLC)确定人参70%乙醇-水提取物中人参皂苷的组成。通过蛋白质印迹分析检测信号激酶的激活情况。

结果

人参70%乙醇-水提取物在TNF-α刺激后显著抑制CXC趋化因子配体10(CXCL-10)的转录和分泌。通过HPLC在我们的提取物中鉴定出9种人参皂苷,包括Rb1、Rb2、Rc、Rd、Re、Rf、Rg1、Rg3和Rh1。9种人参皂苷中的7种可显著抑制U937细胞中TNF-α诱导的CXCL-10表达,并对CXCL-10转录产生与提取物相当的抑制作用。然而,单个人参皂苷对CXCL-10的抑制作用小于粗提物或人参皂苷混合物。CXCL-10的抑制作用可能与人参使细胞外信号调节激酶1/2(ERK1/2)通路失活有关。

结论

我们发现人参抑制了原单核细胞中部分TNF-α诱导的细胞因子和信号蛋白,表明其通过针对TNF-α活性的不同水平发挥抗炎特性。人参的抗炎作用可能归因于人参皂苷的联合作用,这在一定程度上解释了人参在人体中的多种作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/f3b9a3951d52/1479-5876-7-34-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/b9c205117330/1479-5876-7-34-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/e006869d6655/1479-5876-7-34-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/7e8047e691ff/1479-5876-7-34-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/ba288bb14539/1479-5876-7-34-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/f3b9a3951d52/1479-5876-7-34-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/b9c205117330/1479-5876-7-34-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/e006869d6655/1479-5876-7-34-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/7e8047e691ff/1479-5876-7-34-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/ba288bb14539/1479-5876-7-34-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649d/2689162/f3b9a3951d52/1479-5876-7-34-5.jpg

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