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Article: Downregulation of lymphocyte activity and human synovial fibroblast growth in rheumatoid arthritis by triptolide

TitleDownregulation of lymphocyte activity and human synovial fibroblast growth in rheumatoid arthritis by triptolide
Authors
KeywordsAutoimmunity
Chinese herb
Cytotoxicity
Immunosuppression
Triptolide
Issue Date1999
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34597
Citation
Drug Development Research, 1999, v. 47 n. 3, p. 144-153 How to Cite?
AbstractThe antirheumatic effects of triptolide, a purified component derived from a Chinese herb, Tripterygium wilfordii Hook f. (TWH), was examined. Peripheral blood mononuclear cells (PBMC), T cells, or human synovial fibroblasts isolated from healthy controls or rheumatoid arthritis (RA) patients were cultured in vitro in the absence or presence of triptolide. Estimated by ELISA, immunoglobulin synthesis in pokeweed mitogen or Staphylococcus aureus Cowan 1 strain stimulated PBMC was significantly impaired by triptolide in a concentration-dependent manner (1-10 nM). Similarly, proliferation of PBMC in response to phytohemagglutinin (PHA-M), interleukin-2, or phorbol 12-myristate 13-acetate (PMA)/ionomycin estimated by incorporation of [ 3H]-thymidine was inhibited by triptolide. Cell viability was not affected at the immunosuppressive concentrations of triptolide. No abnormality of intracellular Ca 2+ flux as estimated by flow cytometry was detected in PHA-M-stimulated T cells by triptolide. Biosynthesis of cellular protein estimated by incorporation of [ 3H]-leucine was significantly reduced in PMA/ionomycin stimulated PBMC by triptolide at concentrations above 7.5 nM. Proliferation of human synovial fibroblasts as estimated by crystal violet staining was significantly inhibited by triptolide at 30 nM. The present data demonstrate that triptolide is a potent immunosuppressant and has an antiproliferative effect on synovial fibroblast. The immunosuppressive activity of triptolide is not due to cytotoxicity, nor is it targeted at the initial membrane signal transduction process and the generation of second messengers. Inhibition of cellular protein synthesis by triptolide during lymphocyte activation may account for its inhibitory activity. The precise mechanism of action of triptolide needs to be defined in order to develop improved versions of the molecule for the potential treatment of RA.
Persistent Identifierhttp://hdl.handle.net/10722/68869
ISSN
2015 Impact Factor: 0.984
References

 

DC FieldValueLanguage
dc.contributor.authorTong, KKen_HK
dc.contributor.authorYang, Den_HK
dc.contributor.authorChan, EYTen_HK
dc.contributor.authorChiu, PKYen_HK
dc.contributor.authorYau, KSen_HK
dc.contributor.authorLau, CSen_HK
dc.date.accessioned2010-09-06T06:08:28Z-
dc.date.available2010-09-06T06:08:28Z-
dc.date.issued1999en_HK
dc.identifier.citationDrug Development Research, 1999, v. 47 n. 3, p. 144-153en_HK
dc.identifier.issn0272-4391en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68869-
dc.description.abstractThe antirheumatic effects of triptolide, a purified component derived from a Chinese herb, Tripterygium wilfordii Hook f. (TWH), was examined. Peripheral blood mononuclear cells (PBMC), T cells, or human synovial fibroblasts isolated from healthy controls or rheumatoid arthritis (RA) patients were cultured in vitro in the absence or presence of triptolide. Estimated by ELISA, immunoglobulin synthesis in pokeweed mitogen or Staphylococcus aureus Cowan 1 strain stimulated PBMC was significantly impaired by triptolide in a concentration-dependent manner (1-10 nM). Similarly, proliferation of PBMC in response to phytohemagglutinin (PHA-M), interleukin-2, or phorbol 12-myristate 13-acetate (PMA)/ionomycin estimated by incorporation of [ 3H]-thymidine was inhibited by triptolide. Cell viability was not affected at the immunosuppressive concentrations of triptolide. No abnormality of intracellular Ca 2+ flux as estimated by flow cytometry was detected in PHA-M-stimulated T cells by triptolide. Biosynthesis of cellular protein estimated by incorporation of [ 3H]-leucine was significantly reduced in PMA/ionomycin stimulated PBMC by triptolide at concentrations above 7.5 nM. Proliferation of human synovial fibroblasts as estimated by crystal violet staining was significantly inhibited by triptolide at 30 nM. The present data demonstrate that triptolide is a potent immunosuppressant and has an antiproliferative effect on synovial fibroblast. The immunosuppressive activity of triptolide is not due to cytotoxicity, nor is it targeted at the initial membrane signal transduction process and the generation of second messengers. Inhibition of cellular protein synthesis by triptolide during lymphocyte activation may account for its inhibitory activity. The precise mechanism of action of triptolide needs to be defined in order to develop improved versions of the molecule for the potential treatment of RA.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34597en_HK
dc.relation.ispartofDrug Development Researchen_HK
dc.rightsDrug Development Research. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectAutoimmunityen_HK
dc.subjectChinese herben_HK
dc.subjectCytotoxicityen_HK
dc.subjectImmunosuppressionen_HK
dc.subjectTriptolideen_HK
dc.titleDownregulation of lymphocyte activity and human synovial fibroblast growth in rheumatoid arthritis by triptolideen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0272-4391&volume=47&spage=144&epage=153&date=1999&atitle=Downregulation+of+lymphocyte+activity++and+human+synovial+fibroblast+growth+in+rheumatoid+arthritis+by+triptolideen_HK
dc.identifier.emailYang, D:yangdan@hku.hken_HK
dc.identifier.emailChiu, PKY:pkychiu@hkucc.hku.hken_HK
dc.identifier.emailLau, CS:cslau@hku.hken_HK
dc.identifier.authorityYang, D=rp00825en_HK
dc.identifier.authorityChiu, PKY=rp00379en_HK
dc.identifier.authorityLau, CS=rp01348en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/(SICI)1098-2299(199907)47:3<144::AID-DDR5>3.0.CO;2-0en_HK
dc.identifier.scopuseid_2-s2.0-0032805047en_HK
dc.identifier.hkuros50031en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032805047&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume47en_HK
dc.identifier.issue3en_HK
dc.identifier.spage144en_HK
dc.identifier.epage153en_HK
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTong, KK=7102473457en_HK
dc.identifier.scopusauthoridYang, D=7404800756en_HK
dc.identifier.scopusauthoridChan, EYT=7401994013en_HK
dc.identifier.scopusauthoridChiu, PKY=7202988127en_HK
dc.identifier.scopusauthoridYau, KS=7101940494en_HK
dc.identifier.scopusauthoridLau, CS=14035682100en_HK

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