Table 1.
Molecules and Drugs to overcome oxidative stress inducing CVD.
| Nutraceutical/Class of Drug | Main Mechanism of Action | Additional Antioxidative Effects | References |
|---|---|---|---|
| Vitamins and nutraceuticals | |||
| B6 | Metabolic Coenzyme in several cellular processes | Reduction of homocysteine levels | [86] |
| Acid folic (B9) | Metabolic Coenzyme in several cellular processes | (i) Prevention of NOS uncoupling and restoration of endothelial dysfunction (ii) Reduction of homocysteine levels (iii) Heart rate and blood pressure restoration |
[86,91,92,93,94,95] |
| B12 | Metabolic Coenzyme in several cellular processes | (i) Reduction of homocysteine levels (ii) Heart rate and blood pressure restoration |
[86,91,92,93,94,95] |
| C | Antioxidative | Prevention of NOS uncoupling and restoration of endothelial dysfunction | [91,92,93,94] |
| D | Regulation of calcium metabolism | Improvement of cardiac stress and inflammation in obese rats | [96] |
| E | Antioxidative | Restoration of cardiac function and attenuation of atherogenic apo B-48-dependent hyperlipidemia | [97,98,99] |
| Polyphenols | Antioxidative | (i) O2− and peroxynitrite scavenger (ii) Inducers of redox dependent reactions |
[100,101,102] |
| Astaxanthin | Antioxidative | (i) Anti-inflammatory effects (ii) Regulation of lipid and glucose metabolisms |
[103,104,105,106,107] |
| Anti-hypertensives | |||
| Angiotensin converting enzyme (ACE) inhibitors | ACE inhibition | (i) Reduction of monocyte-macrophage recruitment into vessel wall, smooth muscle cells mitogenesis and extracellular matrix storage (ii) Reduction of ACE mediated ROS production (iii) Increase of bradykinin levels |
[91,108,109,110] |
| Angiotensin receptor (AT) blockers | AT blockage | Pleiotropic anti-oxidative effects derived from renin-angiotensin axis blockage without bradykinin-mediated antioxidative effects | [100,101,102,111,112,113,114,115,116] |
| Beta adrenergic receptor blockers | Beta adrenergic receptor blockage | (i) Free radical scavenger function (ii) Decrease of superoxide anions generation (iii) Restoring eNOS expression |
[117,118,119,120,121,122,123,124,125,126,127,128,129,130] |
| Anti-diabetic agents | |||
| Dipeptidyl peptidase-4 (DDP-4) inhibitors | DDP-4 inhibition | (i) Decrease of oxidative burst in whole blood (ii) Decrease of the expression of NADPH oxidase (iii) Elevation cAMP and protein kinase A |
[131,132,133] |
| Glucagon-like peptide-1 (GLP-1) analogues | GLP-1 functions | (i) Decrease of oxidative burst in whole blood (ii) Decrease of the expression of NADPH oxidase (iii) Elevation cAMP and protein kinase A |
[131,132,133] |
| Sodium-glucose cotransporter 2 (SGLT2) inhibitors | SGLT2 blockage | NOS2 and IFNɣ reduction | [131,134] |
| Others | |||
| NO donors | NO and/or NO derived molecule releasing by endothelial cells | NO and/or NO derived molecule releasing by endothelial cells restoring REDOX balance | [92,131,135,136] |
| Statins | 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibition |
(i) Increase of eNOS activity (ii) Decrease of both asymmetrical dimethylarginine levels and NADPH oxidase function |
[91,137,138] |
Abbreviations: ACE: angiotensin converting enzyme, AT: angiotensin receptor, CVD: cardiovascular diseases, DDP-4: Dipeptidyl peptidase-4, eNOS: endothelial NO synthase, GLP-1: glucagon-like peptide-1, NO: nitric oxide, ROS: radical oxygen species, SGLT2: sodium-glucose cotransporter 2.