Semotiadil, a new calcium antagonist, is a very potent inhibitor of LDL-oxidation

Kritz, H; Oguogho, A.; Aghajanian, A. Arakil; Sinzinger, H.

doi:10.1054/plef.1999.0088

Cited by 8 publications

(3 citation statements)

References 32 publications

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“…It was previously reported that calcium channel blockers could inhibit the oxidation of LDL. [44][45][46] Benidipine also has the same action, because the concentration of anti-oxLDL antibody decreased significantly after benidipine treatment in the present study.…”

Section: Discussionsupporting

confidence: 66%

Benidipine improves oxidized LDL-dependent monocyte and endothelial dysfunction in hypertensive patients with type 2 diabetes mellitus

et al. 2005

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We investigated the effects of long-term benidipine treatment on levels of monocyte and endothelial cell activation markers in hypertensive patients with (n ¼ 28) and without (n ¼ 10) type 2 diabetes mellitus. Benidipine, 4 mg/day, was administered for 6 months; there were no other changes in any of the patients pharmacologic regimens during benidipine treatment. Clinical and biochemical data obtained before and after benidipine administration were compared; all markers were measured by ELISA. The levels of platelet activation markers (CD62P, CD63, and PAC-1), microparticles (monocytederived microparticles: MDMPs, and endothelial cellderived microparticles: EDMPs), chemokines (monocyte chemotactic peptide 1: MCP-1, regulated on activation normally T-cell expressed and secreted: RANTES) and soluble adhesion markers (soluble E-selectin and soluble ICAM-1) differed in the control and hypertension groups. In addition, levels of platelet, monocyte, and endothelial cell activation markers, microparticles, chemokines, and soluble adhesion molecules were higher in hypertensive patients than in those without type 2 diabetes. Furthermore, benidipine administration decreased the concentrations of all these markers. The effect of this drug was significant in diabetes patients with high levels of antioxidized low-density lipoprotein (LDL) antibody. These results suggest that benidipine is effective for the treatment of oxLDL-dependent vascular disorders in hypertensive patients with type 2 diabetes.

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Section: Discussionsupporting

confidence: 66%

Benidipine improves oxidized LDL-dependent monocyte and endothelial dysfunction in hypertensive patients with type 2 diabetes mellitus

et al. 2005

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“…These drugs include statins [187,188], calcium channel blockers [189][190][191][192][193], angiotensin II receptor antagonists [194], ACE inhibitors [195][196][197][198][199], compounds such as dobutamine [200], nitric oxide donors [201][202], salicylate [203,204] and many others. Regardless of their action as antioxidants in vivo, their chemical nature as antioxidants cannot be ignored.…”

Section: Antioxidant Activities Of Cardiovascular Drugsmentioning

confidence: 99%

Lipid peroxidation and decomposition — Conflicting roles in plaque vulnerability and stability

Parthasarathy

Litvinov

Selvarajan

et al. 2008

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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The low density lipoprotein (LDL) oxidation hypothesis has generated considerable interest in oxidative stress and how it might affect atherosclerosis. However, the failure of antioxidants, particularly vitamin E, to affect the progression of the disease in humans has convinced even staunch supporters of the hypothesis to take a step backwards and reconsider alternatives.Preponderant evidence for the hypothesis came from animal antioxidant intervention studies. In this review we point out basic differences between animal and human atherosclerosis development and suggest that human disease starts where animal studies end. While initial oxidative steps in the generation of early fatty streak lesions might be common, the differences might be in the steps involved in the decomposition of peroxidized lipids into aldehydes and their further oxidation into carboxylic acids. We suggest that these steps may not be amenable to attenuation by antioxidants and antioxidants might actually counter the stabilization of plaque by preventing the formation of carboxylic acids which are anti-inflammatory in nature. The formation of such dicarboxylic acids may also be conducive to plaque stabilization by trapping calcium.We suggest that agents that would prevent the decomposition of lipid peroxides and promote the formation and removal of lipid hydroxides, such as paraoxonase (PON 1) or apo A1/high density lipoprotein (HDL) might be more conducive to plaque regression. KeywordsAtherosclerosis; aldehydes; dicarboxylation; inflammation; calcification Oxidation hypothesis of atherosclerosisAtherosclerosis is the major manifestation of cardiovascular diseases. The role of lipoproteins in atherosclerosis development has been a topic of interest for over five decades. It is now established beyond doubt that high levels of low density lipoprotein (LDL) and low levels of high density lipoprotein (HDL) contribute significantly to the development and progression of cardiovascular diseases [1][2][3][4][5].The biochemical processes that contributed to the formation of early atherosclerotic lesions, the fatty streak lesions, are still under debate. The LDL oxidation hypothesis was put forward in the eighties to explain the formation of fatty streak lesions and over 4000 publications and countless reviews have appeared on the topic to date [6][7][8][9][10][11] providing evidence for the presence *Address correspondence to: Sampath Parthasarathy, Ph.D., M.B.A*. N-850 Doan Hall, 410 W. 10 th Avenue, Ohio State University, Columbus, OH 43210, Tel: (614) Fax: (614) 292-9259, E-mail: spartha@osumc.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all ...

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“…3a-(Quinoxalin-2-ylmethyl)pyrrolo[2,1-c] [1,4]benzothiazine A (Figure 1) core is a heterocyclic hybrid of two pharmacologically promising scaffolds, 1,4-thiazine [1] and quinoxaline [2]. For example, several heterocyclic compounds with a 1,4-thiazine core were reported to show good antibacterial [3][4][5] and antihypertensive [6][7][8] activities (Figure 1). In addition, several quinoxaline-based structures were used to develop antimicrobial [9] and cytotoxic [10] agents, inhibitors of platelet-derived growth factor receptor tyrosine kinase (PDGFR) [11], acetylcholinesterase (AChE), and butyrylcholinesterase (BChE) [12] (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

3-Benzoyl-2-hydroxy-3a-[(3-methylquinoxalin-2-yl)methyl]-1H-pyrrolo[2,1-c][1,4]benzothiazine-1,4(3aH)-dione

Lystsova,

Khramtsova

2023

Molbank

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Semotiadil, a new calcium antagonist, is a very potent inhibitor of LDL-oxidation

Cited by 8 publications

References 32 publications

Benidipine improves oxidized LDL-dependent monocyte and endothelial dysfunction in hypertensive patients with type 2 diabetes mellitus

Benidipine improves oxidized LDL-dependent monocyte and endothelial dysfunction in hypertensive patients with type 2 diabetes mellitus

Lipid peroxidation and decomposition — Conflicting roles in plaque vulnerability and stability

3-Benzoyl-2-hydroxy-3a-[(3-methylquinoxalin-2-yl)methyl]-1H-pyrrolo[2,1-c][1,4]benzothiazine-1,4(3aH)-dione

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