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

TitleBioactivity-guided identification and cell signaling technology to delineate the immunomodulatory effects of Panax ginseng on human promonocytic U937 cells
Authors
Issue Date2009
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.translational-medicine.com/home/
Citation
Journal Of Translational Medicine, 2009, v. 7 How to Cite?
AbstractBackground: 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-α 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-α 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-α-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-α-inducible cytokines and signalling proteins in promonocytic cells, suggesting that it exerts its anti-inflammatory property targeting at different levels of TNF-α 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. © 2009 Lee et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/125217
ISSN
2023 Impact Factor: 6.1
2023 SCImago Journal Rankings: 1.611
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, DCWen_HK
dc.contributor.authorYang, CLHen_HK
dc.contributor.authorChik, SCCen_HK
dc.contributor.authorLi, JCBen_HK
dc.contributor.authorRong, JHen_HK
dc.contributor.authorChan, GCFen_HK
dc.contributor.authorLau, ASYen_HK
dc.date.accessioned2010-10-31T11:18:08Z-
dc.date.available2010-10-31T11:18:08Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal Of Translational Medicine, 2009, v. 7en_HK
dc.identifier.issn1479-5876en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125217-
dc.description.abstractBackground: 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-α 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-α 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-α-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-α-inducible cytokines and signalling proteins in promonocytic cells, suggesting that it exerts its anti-inflammatory property targeting at different levels of TNF-α 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. © 2009 Lee et al; licensee BioMed Central Ltd.en_HK
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.translational-medicine.com/home/en_HK
dc.relation.ispartofJournal of Translational Medicineen_HK
dc.rightsJournal of Translational Medicine. Copyright © BioMed Central Ltd.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subject.meshChemokine CXCL10 - metabolism-
dc.subject.meshImmunologic Factors - pharmacology-
dc.subject.meshPanax - chemistry-
dc.subject.meshPlant Extracts - pharmacology-
dc.subject.meshSignal Transduction - drug effects-
dc.titleBioactivity-guided identification and cell signaling technology to delineate the immunomodulatory effects of Panax ginseng on human promonocytic U937 cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1479-5876&volume=7, article no. 34&spage=&epage=&date=2009&atitle=Immunomodulatory+effect+of+Panax+ginseng+on+human+promonocytic+U937+cells-
dc.identifier.emailLi, JCB: jamesli@hku.hken_HK
dc.identifier.emailRong, JH: jrong@hku.hken_HK
dc.identifier.emailChan, GCF: gcfchan@hku.hken_HK
dc.identifier.emailLau, ASY: asylau@hku.hken_HK
dc.identifier.authorityLi, JCB=rp00496en_HK
dc.identifier.authorityRong, JH=rp00515en_HK
dc.identifier.authorityChan, GCF=rp00431en_HK
dc.identifier.authorityLau, ASY=rp00474en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1186/1479-5876-7-34en_HK
dc.identifier.pmid19442267-
dc.identifier.pmcidPMC2689162-
dc.identifier.scopuseid_2-s2.0-66949121846en_HK
dc.identifier.hkuros179089en_HK
dc.identifier.hkuros161570-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-66949121846&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.isiWOS:000267240900001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLee, DCW=15751156000en_HK
dc.identifier.scopusauthoridYang, CLH=26668171500en_HK
dc.identifier.scopusauthoridChik, SCC=6507803546en_HK
dc.identifier.scopusauthoridLi, JCB=23103447500en_HK
dc.identifier.scopusauthoridRong, JH=7005980047en_HK
dc.identifier.scopusauthoridChan, GCF=16160154400en_HK
dc.identifier.scopusauthoridLau, ASY=7202626202en_HK
dc.identifier.citeulike4519470-
dc.identifier.issnl1479-5876-

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