Abstract
Objective - We tested the hypothesis that carvedilol, a β-adrenoceptor and α-adrenoceptor antagonist with potent antioxidant property, could inhibit tumor necrosis factor-α (TNF-α)-induced endothelial adhesiveness to human mononuclear cells (MNCs), an early sign of atherogenesis. Methods and Results -Circulating MNCs were isolated from the peripheral blood of healthy subjects. Compared with control condition, pretreatment of carvedilol (10 μmol/L for 18 hours) or probucol (5 μmol/L for 18 hours), but not propanolol, prazosin, or both propanolol and prazosin significantly decreased TNF-α-stimulated adhesiveness of cultured human aortic endothelial cells (HAECs) to MNCs. Carvedilol inhibited TNF-α-stimulated endothelial vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (66.0±2.0% and 55.60±1.0% of control, P
Original language | English |
---|---|
Pages (from-to) | 2075-2081 |
Number of pages | 7 |
Journal | Arteriosclerosis, Thrombosis, and Vascular Biology |
Volume | 24 |
Issue number | 11 |
DOIs | |
Publication status | Published - Nov 2004 |
Externally published | Yes |
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Keywords
- Antioxidant
- Atherosclerosis
- Carvedilol
- Cell adhesion molecules
- Endothelium
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Carvedilol inhibits tumor necrosis factor-α-induced endothelial transcription factor activation, adhesion molecule expression, and adhesiveness to human mononuclear cells. / Chen, Jaw Wen; Lin, Feng Yen; Chen, Yung Hsiang; Wu, Tao Cheng; Chen, Yuh Lien; Lin, Shing Jong.
In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 24, No. 11, 11.2004, p. 2075-2081.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Carvedilol inhibits tumor necrosis factor-α-induced endothelial transcription factor activation, adhesion molecule expression, and adhesiveness to human mononuclear cells
AU - Chen, Jaw Wen
AU - Lin, Feng Yen
AU - Chen, Yung Hsiang
AU - Wu, Tao Cheng
AU - Chen, Yuh Lien
AU - Lin, Shing Jong
PY - 2004/11
Y1 - 2004/11
N2 - Objective - We tested the hypothesis that carvedilol, a β-adrenoceptor and α-adrenoceptor antagonist with potent antioxidant property, could inhibit tumor necrosis factor-α (TNF-α)-induced endothelial adhesiveness to human mononuclear cells (MNCs), an early sign of atherogenesis. Methods and Results -Circulating MNCs were isolated from the peripheral blood of healthy subjects. Compared with control condition, pretreatment of carvedilol (10 μmol/L for 18 hours) or probucol (5 μmol/L for 18 hours), but not propanolol, prazosin, or both propanolol and prazosin significantly decreased TNF-α-stimulated adhesiveness of cultured human aortic endothelial cells (HAECs) to MNCs. Carvedilol inhibited TNF-α-stimulated endothelial vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (66.0±2.0% and 55.60±1.0% of control, P
AB - Objective - We tested the hypothesis that carvedilol, a β-adrenoceptor and α-adrenoceptor antagonist with potent antioxidant property, could inhibit tumor necrosis factor-α (TNF-α)-induced endothelial adhesiveness to human mononuclear cells (MNCs), an early sign of atherogenesis. Methods and Results -Circulating MNCs were isolated from the peripheral blood of healthy subjects. Compared with control condition, pretreatment of carvedilol (10 μmol/L for 18 hours) or probucol (5 μmol/L for 18 hours), but not propanolol, prazosin, or both propanolol and prazosin significantly decreased TNF-α-stimulated adhesiveness of cultured human aortic endothelial cells (HAECs) to MNCs. Carvedilol inhibited TNF-α-stimulated endothelial vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (66.0±2.0% and 55.60±1.0% of control, P
KW - Antioxidant
KW - Atherosclerosis
KW - Carvedilol
KW - Cell adhesion molecules
KW - Endothelium
UR - http://www.scopus.com/inward/record.url?scp=8344234111&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=8344234111&partnerID=8YFLogxK
U2 - 10.1161/01.ATV.0000145016.69181.fa
DO - 10.1161/01.ATV.0000145016.69181.fa
M3 - Article
C2 - 15374848
AN - SCOPUS:8344234111
VL - 24
SP - 2075
EP - 2081
JO - Arteriosclerosis, Thrombosis, and Vascular Biology
JF - Arteriosclerosis, Thrombosis, and Vascular Biology
SN - 1079-5642
IS - 11
ER -