The influence of propofol on the expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in reoxygenated human umbilical vein endothelial cells.

Hdl Handle:
http://hdl.handle.net/10147/208833
Title:
The influence of propofol on the expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in reoxygenated human umbilical vein endothelial cells.
Authors:
Corcoran, T B; Engel, A; Shorten, G D
Affiliation:
Cork University Hospital, Department of Anaesthesia, Cork City, Republic of, IrelandUniversity College Cork, Department of Anaesthesia, Cork City, Republic of, Ireland. mascor@gofree.indigo.ie
Citation:
Eur J Anaesthesiol. 2006 Nov;23(11):942-7. Epub 2006 Jul 11.
Journal:
European journal of anaesthesiology
Issue Date:
3-Feb-2012
URI:
http://hdl.handle.net/10147/208833
DOI:
10.1017/S0265021506000846
PubMed ID:
16834788
Abstract:
BACKGROUND: Leucocytes are a pivotal component of the inflammatory cascade that results in tissue injury in a large group of disorders. Free radical production and endothelial activation promote leucocyte-endothelium interactions via endothelial expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) which augment these processes, particularly in the setting of reperfusion injury. Propofol has antioxidant properties which may attenuate the increased expression of these molecules that is observed. METHODS: Cultured human umbilical vein endothelial cells were exposed to 20 h of hypoxia, then returned to normoxic conditions. Cells were treated with saline, Diprivan 5 microg mL(-1) or propofol 5 microg mL(-1), for 4 h after reoxygenation and were examined for ICAM-1 and VCAM-1 expression. RESULTS: Hypoxia did not increase the expression of ICAM-1/VCAM-1. ICAM-1 expression peaked 12 h after reoxygenation (21.75(0.6) vs. 9.6(1.3), P = 0.02). Propofol, but not Diprivan, prevented this increase (8.2(2.9) vs. 21.75(0.6), P = 0.009). VCAM-1 expression peaked 24 h after reoxygenation (9.8(0.9) vs. 6.6(0.6), P = 0.03). Propofol and Diprivan prevented this increase, with no difference between the two treatments observed (4.3(0.3) and 6.4(0.5) vs. 9.8(0.9), P = 0.001, 0.02, respectively). CONCLUSION: These effects are likely to be attributable to the antioxidant properties of propofol, and suggest that propofol may have a protective role in disorders where free radical mediated injury promotes leucocyte-endothelium adhesive interactions.
Language:
eng
MeSH:
Analysis of Variance; Anesthetics, Intravenous/*therapeutic use; Cell Hypoxia/physiology; Cells, Cultured; Endothelial Cells/*drug effects/metabolism; Endothelium, Vascular/cytology; Humans; Intercellular Adhesion Molecule-1/*metabolism; Leukocytes/immunology; Oxygen/metabolism; Propofol/*therapeutic use; Time Factors; Umbilical Veins; Vascular Cell Adhesion Molecule-1/*metabolism
ISSN:
0265-0215 (Print); 0265-0215 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorCorcoran, T Ben_GB
dc.contributor.authorEngel, Aen_GB
dc.contributor.authorShorten, G Den_GB
dc.date.accessioned2012-02-03T15:04:51Z-
dc.date.available2012-02-03T15:04:51Z-
dc.date.issued2012-02-03T15:04:51Z-
dc.identifier.citationEur J Anaesthesiol. 2006 Nov;23(11):942-7. Epub 2006 Jul 11.en_GB
dc.identifier.issn0265-0215 (Print)en_GB
dc.identifier.issn0265-0215 (Linking)en_GB
dc.identifier.pmid16834788en_GB
dc.identifier.doi10.1017/S0265021506000846en_GB
dc.identifier.urihttp://hdl.handle.net/10147/208833-
dc.description.abstractBACKGROUND: Leucocytes are a pivotal component of the inflammatory cascade that results in tissue injury in a large group of disorders. Free radical production and endothelial activation promote leucocyte-endothelium interactions via endothelial expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) which augment these processes, particularly in the setting of reperfusion injury. Propofol has antioxidant properties which may attenuate the increased expression of these molecules that is observed. METHODS: Cultured human umbilical vein endothelial cells were exposed to 20 h of hypoxia, then returned to normoxic conditions. Cells were treated with saline, Diprivan 5 microg mL(-1) or propofol 5 microg mL(-1), for 4 h after reoxygenation and were examined for ICAM-1 and VCAM-1 expression. RESULTS: Hypoxia did not increase the expression of ICAM-1/VCAM-1. ICAM-1 expression peaked 12 h after reoxygenation (21.75(0.6) vs. 9.6(1.3), P = 0.02). Propofol, but not Diprivan, prevented this increase (8.2(2.9) vs. 21.75(0.6), P = 0.009). VCAM-1 expression peaked 24 h after reoxygenation (9.8(0.9) vs. 6.6(0.6), P = 0.03). Propofol and Diprivan prevented this increase, with no difference between the two treatments observed (4.3(0.3) and 6.4(0.5) vs. 9.8(0.9), P = 0.001, 0.02, respectively). CONCLUSION: These effects are likely to be attributable to the antioxidant properties of propofol, and suggest that propofol may have a protective role in disorders where free radical mediated injury promotes leucocyte-endothelium adhesive interactions.en_GB
dc.language.isoengen_GB
dc.subject.meshAnalysis of Varianceen_GB
dc.subject.meshAnesthetics, Intravenous/*therapeutic useen_GB
dc.subject.meshCell Hypoxia/physiologyen_GB
dc.subject.meshCells, Cultureden_GB
dc.subject.meshEndothelial Cells/*drug effects/metabolismen_GB
dc.subject.meshEndothelium, Vascular/cytologyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshIntercellular Adhesion Molecule-1/*metabolismen_GB
dc.subject.meshLeukocytes/immunologyen_GB
dc.subject.meshOxygen/metabolismen_GB
dc.subject.meshPropofol/*therapeutic useen_GB
dc.subject.meshTime Factorsen_GB
dc.subject.meshUmbilical Veinsen_GB
dc.subject.meshVascular Cell Adhesion Molecule-1/*metabolismen_GB
dc.titleThe influence of propofol on the expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in reoxygenated human umbilical vein endothelial cells.en_GB
dc.contributor.departmentCork University Hospital, Department of Anaesthesia, Cork City, Republic of, IrelandUniversity College Cork, Department of Anaesthesia, Cork City, Republic of, Ireland. mascor@gofree.indigo.ieen_GB
dc.identifier.journalEuropean journal of anaesthesiologyen_GB
dc.description.provinceMunster-
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