Antioxidants and Atherosclerosis: Mechanistic Aspects

Abstract

Atherosclerosis is a chronic inflammatory disease which is a major cause of coronary heart disease and stroke in humans. It is characterized by intimal plaques and cholesterol accumulation in arterial walls. The side effects of currently prescribed synthetic drugs and their high cost in the treatment of atherosclerosis has prompted the use of alternative herbal medicines, dietary supplements, and antioxidants associated with fewer adverse effects for the treatment of atherosclerosis. This article aims to present the activity mechanisms of antioxidants on atherosclerosis along with a review of the most prevalent medicinal plants employed against this multifactorial disease. The wide-ranging information in this review article was obtained from scientific databases including PubMed, Web of Science, Scopus, Science Direct and Google Scholar. Natural and synthetic antioxidants have a crucial role in the prevention and treatment of atherosclerosis through different mechanisms. These include: The inhibition of low density lipoprotein (LDL) oxidation, the reduction of reactive oxygen species (ROS) generation, the inhibition of cytokine secretion, the prevention of atherosclerotic plaque formation and platelet aggregation, the preclusion of mononuclear cell infiltration, the improvement of endothelial dysfunction and vasodilation, the augmentation of nitric oxide (NO) bioavailability, the modulation of the expression of adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on endothelial cells, and the suppression of foam cell formation.

<p>Inhibitory Effect of Curcumin on Artery Restenosis Following Carotid Endarterectomy and Its Associated Mechanism in vitro and in vivo</p>

“…26 ROS has been recognized as an important signaling pathway in the proliferation of VSMCs, which is closely associated with the pathophysiological processes of atherosclerosis and restenosis. 27,28 The results of the present study indicated that Cur could inhibit cell viability, inflammatory and oxidative stress responses and induce apoptosis of CCC-SMC-1 cells treated with Ang II, which was consistent with previous studies. In addition, Jang HS et al demonstrated that Cur may be a safer and more effective method to prevent restenosis in a hypercholesterolemic rabbit Iliac artery stent model.…”

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

“…Moreover, in a study not included in the previously cited meta-analysis, CoQ 10 supplementation at a dosage of 100 mg/day for 12 weeks had positive effects on insulin metabolism and MDA levels among diabetic nephropathy patients yet fasting glucose remained unchanged [144]. Finally, a recent meta-analysis of 4 RCTs and 4 experimental studies of diabetic people revealed that CoQ 10 CoQ 10 supplementation for diabetic hemodialysis patients for 12 weeks did not influence lipid profiles [70,146,147]. In hemodialysis patients, 100 mg/day of CoQ 10 for 3 months could significantly reduce CRP levels (95%CI = −20.1 to −10.5, p < 0.001) [148], while daily supplementation with 1200 mg of CoQ 10 significantly improved biomarkers of oxidative stress [149].…”

“…CoQ 10 , in its reduced form, has been shown to inhibit the peroxidation of cell membrane lipids and to reduce the oxidation of circulating lipids. Interestingly, in vitro, it inhibits the oxidation of low-density lipoprotein more than other antioxidant molecules, such as α-tocopherol or β-carotene [9,10].…”

Pathological Roles of Mitochondrial Oxidative Stress and Mitochondrial Dynamics in Cardiac Microvascular Ischemia/Reperfusion Injury

“…Catalase in the mitochondrial matrix can also convert H 2 O 2 into water and molecular oxygen [86,87]. Glutathione biosynthesis is catalyzed by glutathione reductase using the oxidation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) into NADP and is crucial in antioxidant activities in the mitochondria [88,89] Another important source of ROS in the re-perfused heart are the two isoforms of monoamine oxidases (MAO), MAO-A and MAO-B, which are located on the outer mitochondrial membrane [92]. It has been demonstrated that MAO-A activity is enhanced by I/R injury and is responsible for the precipitation of hydrogen peroxide and the progression towards left ventricle hypertrophy and cardiac remodeling [93].…”