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- Publisher Website: 10.3233/CH-2010-1269
- Scopus: eid_2-s2.0-77954100567
- PMID: 20571239
- WOS: WOS:000279013700002
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Article: The effect of salvianolic acid B combined with laminar shear stress on TNF-α-stimulated adhesion molecule expression in human aortic endothelial cells
Title | The effect of salvianolic acid B combined with laminar shear stress on TNF-α-stimulated adhesion molecule expression in human aortic endothelial cells | ||||||||
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Authors | |||||||||
Keywords | adhesion molecules IκBα laminar shear stress NF-κB salvianolic acid B TNF-α | ||||||||
Issue Date | 2010 | ||||||||
Publisher | IOS 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? | ||||||||
Abstract | The 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 Identifier | http://hdl.handle.net/10722/147621 | ||||||||
ISSN | 2023 Impact Factor: 2.1 2023 SCImago Journal Rankings: 0.456 | ||||||||
ISI Accession Number ID |
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 Field | Value | Language |
---|---|---|
dc.contributor.author | Xie, LX | en_US |
dc.contributor.author | Durairajan, SSK | en_US |
dc.contributor.author | Lu, JH | en_US |
dc.contributor.author | Liu, CL | en_US |
dc.contributor.author | Kum, WF | en_US |
dc.contributor.author | Wang, Y | en_US |
dc.contributor.author | Koo, I | en_US |
dc.contributor.author | Wu, WK | en_US |
dc.contributor.author | Han, D | en_US |
dc.contributor.author | Lao, F | en_US |
dc.contributor.author | Huang, JD | en_US |
dc.contributor.author | Li, M | en_US |
dc.date.accessioned | 2012-05-29T06:05:02Z | - |
dc.date.available | 2012-05-29T06:05:02Z | - |
dc.date.issued | 2010 | en_US |
dc.identifier.citation | Clinical Hemorheology And Microcirculation, 2010, v. 44 n. 4, p. 245-258 | en_US |
dc.identifier.issn | 1386-0291 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/147621 | - |
dc.description.abstract | The 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.language | eng | en_US |
dc.publisher | IOS Press. The Journal's web site is located at http://www.iospress.nl/html/13860291.php | en_US |
dc.relation.ispartof | Clinical Hemorheology and Microcirculation | en_US |
dc.subject | adhesion molecules | - |
dc.subject | IκBα | - |
dc.subject | laminar shear stress | - |
dc.subject | NF-κB | - |
dc.subject | salvianolic acid B | - |
dc.subject | TNF-α | - |
dc.subject.mesh | Anti-Inflammatory Agents - Pharmacology | en_US |
dc.subject.mesh | Benzofurans | en_US |
dc.subject.mesh | Cell Adhesion - Drug Effects | en_US |
dc.subject.mesh | E-Selectin - Biosynthesis | en_US |
dc.subject.mesh | Endothelium, Vascular - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Intercellular Adhesion Molecule-1 - Biosynthesis | en_US |
dc.subject.mesh | Nf-Kappa B - Metabolism | en_US |
dc.subject.mesh | Signal Transduction - Drug Effects | en_US |
dc.subject.mesh | Stress, Mechanical | en_US |
dc.subject.mesh | Tumor Necrosis Factor-Alpha - Pharmacology | en_US |
dc.subject.mesh | U937 Cells - Drug Effects | en_US |
dc.subject.mesh | Vascular Cell Adhesion Molecule-1 - Biosynthesis | en_US |
dc.title | The effect of salvianolic acid B combined with laminar shear stress on TNF-α-stimulated adhesion molecule expression in human aortic endothelial cells | en_US |
dc.type | Article | en_US |
dc.identifier.email | Huang, JD:jdhuang@hkucc.hku.hk | en_US |
dc.identifier.authority | Huang, JD=rp00451 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.3233/CH-2010-1269 | en_US |
dc.identifier.pmid | 20571239 | - |
dc.identifier.scopus | eid_2-s2.0-77954100567 | en_US |
dc.identifier.hkuros | 179185 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-77954100567&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 44 | en_US |
dc.identifier.issue | 4 | en_US |
dc.identifier.spage | 245 | en_US |
dc.identifier.epage | 258 | en_US |
dc.identifier.isi | WOS:000279013700002 | - |
dc.publisher.place | Netherlands | en_US |
dc.identifier.scopusauthorid | Xie, LX=23483050700 | en_US |
dc.identifier.scopusauthorid | Durairajan, SSK=23469201000 | en_US |
dc.identifier.scopusauthorid | Lu, JH=16175647100 | en_US |
dc.identifier.scopusauthorid | Liu, CL=24503690100 | en_US |
dc.identifier.scopusauthorid | Kum, WF=15063144400 | en_US |
dc.identifier.scopusauthorid | Wang, Y=36519749900 | en_US |
dc.identifier.scopusauthorid | Koo, I=23469778400 | en_US |
dc.identifier.scopusauthorid | Wu, WK=35084725300 | en_US |
dc.identifier.scopusauthorid | Han, D=15821708500 | en_US |
dc.identifier.scopusauthorid | Lao, F=36519215700 | en_US |
dc.identifier.scopusauthorid | Huang, JD=8108660600 | en_US |
dc.identifier.scopusauthorid | Li, M=36071647500 | en_US |
dc.identifier.issnl | 1386-0291 | - |