Table 2.
Antioxidant | Model | Dose | Results | Ref. | |
---|---|---|---|---|---|
Vit E α-tocopherol (C29H50O2) |
C57BL/6 mice (in vivo) | 2.5 mg/kg BW in 0.8% DMSO 2 h prior to surgery, immediately after PCI, and twice per day for three consecutive days | ↓ Infarct size ↓ ROS and lipid oxidation ↓ MPO activity ↓ Neutrophil infiltration Prevented pathological changes |
[101] | |
Langendorff model using male Hartley Guinea pigs hearts (ex vivo) | 100 μM | QT segment recovered 10% | [102] | ||
NAC (C5H9NO3S) NAC (C5H9NO3S) |
Human (in vivo) | IV bolus of 1200 mg before PCI and 1200 mg IV twice daily for the 48 h after PCI (total dose 6000 mg) | ↓ Oxidative stress It does not provide an additional clinical benefit to placebo with respect to patients undergoing PCI. No adverse effects. |
[103] | |
Human (in vivo) |
Patients with AMI received 15 g infused over 24 h + IV NTG and streptokinase |
↓ Oxidative stress. NAC and GSH concentration were correlated. ↓ MDA concentrations over the first 8 h of treatment. Better preservation of LV function. No adverse effects. |
[104] | ||
Human (in vivo) | NAC 100 mg/kg bolus followed by intracoronary NAC 480 mg during PCI then IV NAC 10 mg/kg for 12 h |
↓ Peak hs-TnT level after PCI. Difference in peak CK-MB was not statistically significant. No adverse effects |
[105] | ||
Human (in vivo) |
Infusion of 50 mg/kg, followed by IV infusion for 48 h after the operation at a dose of 50 mg/kg/day | ↓ Rate of atrial fibrillation in the NAC group. | [106] | ||
DFO (C25H48N6O8) |
Human (in vivo) |
4 g were infused for 8 h | Prevented ROS production Improved LVEF No major cardiac event was reported with long term administration |
[107] | |
Human (in vivo) |
500 mg 5 to 10 min before PCI, followed by 50 mg/kg over 12 h | ↓ Serum iron and plasma F2-isoprostane levels during the first hours. No changes in the infarct size. |
[108] | ||
Polyphenols (Flavonols) |
Quercetin (C15H10O7) |
Cells suspension of rats (Wistar strain) Thymocytes (in vitro) |
2 mL cell suspension in a 10 mL test tube | Protective effect on the cells suffering oxidative stress and cells suffering from intracellular Ca2+ overload. ↓ Cell death |
[109] |
Langendorff model using male Wistar rat hearts (ex vivo) |
15 µM | Improvement in the functional parameters of the heart (LVDP and contractility) ↓ End-diastolic pressure. |
[110] | ||
Human (in vivo) |
500 mg twice daily for 1 month | ↓ Inflammation | [111] | ||
Polyphenols (Stilbenes) |
Resveratrol (C14H12O3) |
Male rats (Sprague-Dawley) (in vivo) |
100 µM | ↓ Infarct size, ↓ Myocardial apoptosis ↓ NF-κB expression ↓ Neutrophil infiltration ↓ TNF-α levels ↓ Cardiac dysfunction ↓ Activity of serum CK-MB and LDH level ↓ MDA levels ↑ Antioxidant enzymes activities ↑ Nrf2 and HO-1 |
[112,113] |
Male rats (Sprague-Dawley) (in vivo) |
2.5, 5, and 10 mg/kg | ↓ Necrotic area ↓ TnT and CK-MB release ↓ IL-1β and IL-18 release ↓ Myocardial NALP3 expression Inhibits I/R-mediated myocardial Caspase1 expression. |
[114] | ||
Polyphenols (Anthocyanins) |
C3OG (C21H21O11+, Cl−) |
Langendorff model (ex vivo) using hearts from male rats (Wistar) | 20 μM | ↓ Cardiomyocyte death ↓ LDH levels Protection against apoptosis induced by I/R Cytochrome c-reducing activity Stimulation of mitochondrial respiration after ischemia |
[115] |
40 μM | No significant changes compared to 20 μM of C3OG | ||||
P3OG (C21H21O10+) |
Langendorff model (ex vivo) using hearts from male rats (Wistar) | 20 μM | Cardiomyocyte death was not statistically different from the I/R control group ↑ LDH activity than in the control group and similar to the I/R group |
||
40 μM | No significant changes compared to 20 μM of P3GO |
AMI, acute myocardial infarction; C3OG, Cyanidin-3-O-glucoside; CK-MB, creatinine phosphokinase MB isoenzyme; DFO, deferoxamine; DMSO, dimethylsulfoxide; GSH, reduced glutathione; HO-1, heme oxygenase-1; IL, Interleukin; IV, instravenously LDH, lactate dehydrogenase; LV, left ventricule; LVDP, left ventricular diastolic pressure; LVEF, left ventricular ejection fraction; MDA, Malondialdehyde; MPO, Myeloperoxidase; NAC, N-acetylcysteine; NALP3, NLRP3 inflammasome; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; NTG, nitroglycerin; Nrf2, nuclear factor-erythroid 2-related factor 2; P3OG, Pelargonidin-3-O-glucoside; PCI, percutaneous coronary intervention; ROS, reactive oxygen species; TNF-α, tumor necrosis factor alpha; TnT, troponin T; Vit E, vitamin E; ↑, increase; ↓, decrease.