File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The effect of salvianolic acid B combined with laminar shear stress on TNF-α-stimulated adhesion molecule expression in human aortic endothelial cells

TitleThe effect of salvianolic acid B combined with laminar shear stress on TNF-α-stimulated adhesion molecule expression in human aortic endothelial cells
Authors
Issue Date2010
PublisherIOS Press. The Journal's web site is located at http://www.iospress.nl/html/13860291.php
Citation
Clinical Hemorheology And Microcirculation, 2010, v. 44 n. 4, p. 245-258 How to Cite?
AbstractThe study was conducted to investigate the effect of Salvianolic acid B (Sal B) on TNF-α-stimulated adhesion molecule expression i.e. vascular adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and E-selectin in human aortic endothelial cells (HAECs) under laminar shear stress (LSS) condition. Exposure of HAECs to LSS (12 dynes/cm2 for 6 h decreased the TNF-α-induced protein expression of adhesion molecules i.e. VCAM-1, ICAM-1 and E-selectin. Pre-treatment of HAECs with Sal B (10 μg/ml) then exposed to LSS (12 dynes/cm2) for 6 h significantly inhibited VCAM-1, ICAM-1 and E-selectin expression stimulated by TNF-α. Moreover, combined Sal B and LSS treatment inhibited the adhesiveness of monocytic U937 cells to TNF-α-stimulated HAECs. We further examined the molecular mechanisms and found that the combination of Sal B and LSS treatment dramatically inhibited TNF-α-induced NF-κB activation evidenced by IκBα degradation and p65 nuclear translocation in HAECs. This study provides the first biomechanopharmacological evidence that Sal B has a combination effect with LSS to reduce the expression of three adhesion molecules, leading to reduced monocyte adhesion to HAECs, at least in part, by inhibiting the NF-κB signaling pathway. Data from this study thus support the potential clinical application of Sal B in vascular inflammatory diseases. © 2010 - IOS Press and the authors. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/147621
ISSN
2015 Impact Factor: 1.815
2015 SCImago Journal Rankings: 0.665
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Baptist UniversityFRG/05-06/II-24
FRG/07-08/II-51
FRG/08-09/II-19
Eu Yan Sang (Hong Kong) LimitedEYS/07-08/01
NSFC12672192
Funding Information:

This work was supported by faculty research grants FRG/05-06/II-24, FRG/07-08/II-51 and FRG/08-09/II-19 from Hong Kong Baptist University, also supported in part by grant EYS/07-08/01 from Eu Yan Sang (Hong Kong) Limited, and this work is linked with NSFC project (12672192). We thank Dr. Jeng-Jian Chiu and Ms. Li-Jing Chen from Division of Medical Engineering Research of National Health Research Institutes in Taiwan for their valuable suggestions and technical support on this project.

References

 

DC FieldValueLanguage
dc.contributor.authorXie, LXen_US
dc.contributor.authorDurairajan, SSKen_US
dc.contributor.authorLu, JHen_US
dc.contributor.authorLiu, CLen_US
dc.contributor.authorKum, WFen_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorKoo, Ien_US
dc.contributor.authorWu, WKen_US
dc.contributor.authorHan, Den_US
dc.contributor.authorLao, Fen_US
dc.contributor.authorHuang, JDen_US
dc.contributor.authorLi, Men_US
dc.date.accessioned2012-05-29T06:05:02Z-
dc.date.available2012-05-29T06:05:02Z-
dc.date.issued2010en_US
dc.identifier.citationClinical Hemorheology And Microcirculation, 2010, v. 44 n. 4, p. 245-258en_US
dc.identifier.issn1386-0291en_US
dc.identifier.urihttp://hdl.handle.net/10722/147621-
dc.description.abstractThe study was conducted to investigate the effect of Salvianolic acid B (Sal B) on TNF-α-stimulated adhesion molecule expression i.e. vascular adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and E-selectin in human aortic endothelial cells (HAECs) under laminar shear stress (LSS) condition. Exposure of HAECs to LSS (12 dynes/cm2 for 6 h decreased the TNF-α-induced protein expression of adhesion molecules i.e. VCAM-1, ICAM-1 and E-selectin. Pre-treatment of HAECs with Sal B (10 μg/ml) then exposed to LSS (12 dynes/cm2) for 6 h significantly inhibited VCAM-1, ICAM-1 and E-selectin expression stimulated by TNF-α. Moreover, combined Sal B and LSS treatment inhibited the adhesiveness of monocytic U937 cells to TNF-α-stimulated HAECs. We further examined the molecular mechanisms and found that the combination of Sal B and LSS treatment dramatically inhibited TNF-α-induced NF-κB activation evidenced by IκBα degradation and p65 nuclear translocation in HAECs. This study provides the first biomechanopharmacological evidence that Sal B has a combination effect with LSS to reduce the expression of three adhesion molecules, leading to reduced monocyte adhesion to HAECs, at least in part, by inhibiting the NF-κB signaling pathway. Data from this study thus support the potential clinical application of Sal B in vascular inflammatory diseases. © 2010 - IOS Press and the authors. All rights reserved.en_US
dc.languageengen_US
dc.publisherIOS Press. The Journal's web site is located at http://www.iospress.nl/html/13860291.phpen_US
dc.relation.ispartofClinical Hemorheology and Microcirculationen_US
dc.subject.meshAnti-Inflammatory Agents - Pharmacologyen_US
dc.subject.meshBenzofuransen_US
dc.subject.meshCell Adhesion - Drug Effectsen_US
dc.subject.meshE-Selectin - Biosynthesisen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshIntercellular Adhesion Molecule-1 - Biosynthesisen_US
dc.subject.meshNf-Kappa B - Metabolismen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshStress, Mechanicalen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Pharmacologyen_US
dc.subject.meshU937 Cells - Drug Effectsen_US
dc.subject.meshVascular Cell Adhesion Molecule-1 - Biosynthesisen_US
dc.titleThe effect of salvianolic acid B combined with laminar shear stress on TNF-α-stimulated adhesion molecule expression in human aortic endothelial cellsen_US
dc.typeArticleen_US
dc.identifier.emailHuang, JD:jdhuang@hkucc.hku.hken_US
dc.identifier.authorityHuang, JD=rp00451en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.3233/CH-2010-1269en_US
dc.identifier.pmid20571239-
dc.identifier.scopuseid_2-s2.0-77954100567en_US
dc.identifier.hkuros179185-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77954100567&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume44en_US
dc.identifier.issue4en_US
dc.identifier.spage245en_US
dc.identifier.epage258en_US
dc.identifier.isiWOS:000279013700002-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridXie, LX=23483050700en_US
dc.identifier.scopusauthoridDurairajan, SSK=23469201000en_US
dc.identifier.scopusauthoridLu, JH=16175647100en_US
dc.identifier.scopusauthoridLiu, CL=24503690100en_US
dc.identifier.scopusauthoridKum, WF=15063144400en_US
dc.identifier.scopusauthoridWang, Y=36519749900en_US
dc.identifier.scopusauthoridKoo, I=23469778400en_US
dc.identifier.scopusauthoridWu, WK=35084725300en_US
dc.identifier.scopusauthoridHan, D=15821708500en_US
dc.identifier.scopusauthoridLao, F=36519215700en_US
dc.identifier.scopusauthoridHuang, JD=8108660600en_US
dc.identifier.scopusauthoridLi, M=36071647500en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats