| Autor: |
Van Antwerpen P; Laboratory of Pharmaceutical Chemistry, Institute of Pharmacy, Université Libre de Bruxelles, Campus Plaine 205-5, B-1050 Brussels, Belgium., Legssyer I, Zouaoui Boudjeltia K, Babar S, Moreau P, Moguilevsky N, Vanhaeverbeek M, Ducobu J, Nève J |
| Jazyk: |
angličtina |
| Zdroj: |
European journal of pharmacology [Eur J Pharmacol] 2006 May 10; Vol. 537 (1-3), pp. 31-6. Date of Electronic Publication: 2006 Mar 20. |
| DOI: |
10.1016/j.ejphar.2006.03.022 |
| Abstrakt: |
The oxidative modification of low-density lipoproteins (LDL) is a key event in the formation of atheromatous lesions. Indeed, oxidized derivatives accumulate in the vascular wall and promote a local inflammatory process which triggers the progression of the atheromatous plaque. Myeloperoxidase (MPO) has been mentioned as a major contributor to this oxidative process. It takes part in the oxidation both of lipids by chlorination and peroxidation and of apolipoprotein B-100. Based on recent observations with several anti-inflammatory and thiol-containing drugs, the present study was designed to test the hypothesis that anti-hypertensive agents from the angiotensin converting enzyme (ACE) inhibitors group inhibit the oxidative modifications of Apo B-100 caused by MPO. Captopril, ramipril, enalapril, lisinopril and fosinopril were assessed by measuring: their inhibiting effect on the MPO/H(2)O(2)/Cl(-) system, the accumulation of compound II, which reflects the inhibition of the synthesis of HOCl and the LDL oxidation by MPO in presence of several concentrations of ACE inhibitors. Only captopril, a thiol-containing ACE inhibitor, was able to significantly decrease the oxidative modification of LDL in a dose dependent manner and this by scavenging HOCl. This efficient anti-hypertensive drug therefore appears to also protect against the atherosclerotic process by this newly documented mechanism. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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