Table 1.
Summary of antioxidant activities and underlying mechanisms of raspberry ketone (RK).
| Mechanism(s) | Dose | Study Model | Study Result(s) | Ref. | |
|---|---|---|---|---|---|
| TAC↑ | 25, 50, 100 and 200 mg/kg | Male Wistar rats induced hepatotoxicity by CCl4 | Dose-dependent amelioration of TAC by RK treatment, which was decreased by half in the toxic group | [57] | |
| 50, 100 and 200 mg/kg | Wistar albino rats induced cardiotoxicity with ISO | Dose-dependent upregulation of TAC (3.914 ± 0.65 to 9.509 ± 0.84 µmol/L) by RK treatment compared with that in the ISO-treated group (2.598 ± 0.77 µmol/L) | [59] | ||
| 44 mg/kg | High-fat diet-fed male Wister albino rats | Increased TAC (0.7 ± 0.05 mg/dL) by RK treatment compared with that in the obese group (0.423 ± 0.03 mg/dL) | [61] | ||
| Antioxidant Enzyme Activity |
SOD↑ | 0.5%, 1% or 2% | High-fat diet-fed male female Sprague-Dawley rats | RK high-dose group normalized SOD activity, which was reduced by about 33% with a high-fat diet | [56] |
| 25, 50, 100 and 200 mg/kg | Male Wistar rats induced hepatotoxicity by CCl4 | RK at 200 mg/kg normalized the SOD activity, which was dropped by about 50% due to CCl4 | [57] | ||
| 50, 100 and 200 mg/kg | Wistar albino rats induced myocardial by ISO | Significant increases in SOD level in medium- (100 mg/kg) and high-dose (200 mg/kg) of RK groups (58.39 ± 1.28 and 59.52 ± 2.3 U/mg protein, respectively) compared with that in the ISO-treated group (28.77 ± 1.4 U/mg protein) | [62] | ||
| 6 mg/kg | Male albino rats induced toxicity by AA | RK co-treatment improved the SOD level (128.26 ± 6.34 U/mL) compared with that in AA-treated group (75.65 ± 5.87 U/mL) | [63] | ||
| 25, 50, 100 and 200 mg/kg | Adult male Swiss albino rats induced pulmonary toxicity by CP | Dose-dependent recovery of SOD level (55.32 ± 2.42, 56.28 ± 2.30, 68.36 ± 3.89, and 74.59 ± 2.15 U/mg protein, respectively) by RK pre-treatment against CP-induced toxicity (40.51 U/mg protein) | [64] | ||
| CAT↑ | 50 mg/kg | Adult male Wistar rats induced gastric lesion by EtOH | CAT was abated with EtOH treatment (3.7 ± 0.07 U/g tissue); RK treatment reversed the CAT level (6.2 ± 0.28 U/g tissue) | [54] | |
| 50, 100 and 200 mg/kg | Wistar albino rats induced myocardial by ISO | Significant increases in CAT level in medium- and high-dose of RK groups (37.44 ± 2.92 and 37.95 ± 2.35 nmol H2O2/min/mg protein, respectively) compared with that in the ISO-treated group (14.75 ± 1.98 nmol H2O2/min/mg protein) | [62] | ||
| 6 mg/kg | Adult male albino rats induced toxicity by AA | RK co-treatment improved the CAT level (4.13 ± 0.45 U/mL) compared with that in AA-treated group (2.57 ± 0.64 U/mL) | [63] | ||
| 25, 50, 100 and 200 mg/kg | Adult male Swiss albino rats induced pulmonary toxicity by CP | Dose-dependent recovery of CAT level (84.31 ± 4.75, 89.31 ± 1.70, 116.32 ± 12.25, and 128.59 ± 9.30 U/mg protein, respectively) by RK pre-treatment against CP-induced toxicity (59.86 ± 4.72 U/mg protein) | [64] | ||
| GSH-Px↑ | 50 mg/kg | Adult male Wistar rats induced gastric lesion by EtOH | Significant amelioration of GSH-Px activity (262 ± 15.7 U/g tissue) compared with that in the EtOH group (86.8 ± 5.6 U/g tissue) | [54] | |
| Lipid peroxidation |
GSH↑ | 50 mg/kg | Adult male Wistar rats induced gastric lesion by EtOH | Significant decrease in GSH content in the EtOH-treated group (2.8 ± 0.18 µmol/g tissue) compared with that in the control group (7.1 ± 0.43 µmol/g tissue); RK normalized the GSH content (7.8 ± 0.21 µmol/g tissue) | [54] |
| 25, 50, 100 and 200 mg/kg | Male Wistar rats induced hepatotoxicity by CCl4 | Dose-dependent recovery in GSH levels by RK treatment, which was reduced by 40% due to CCl4 | [57] | ||
| 50, 100 and 200 mg/kg | Wistar albino rats induced myocardial by ISO | Significant elevations in GSH level in medium- and high-dose of RK groups (3.88 ± 0.08 and 4.07 ± 0.18 µmol GSH/mg protein, respectively) compared with that in the ISO-treated group (0.97 ± 0.15 µmol GSH/mg protein) | [62] | ||
| 250 and 500 mg/kg | High-fat diet-fed Male Wistar albino rats | RK treatment 2-fold increased the content of GSH, compared with that in the obese group | [65] | ||
| 55 mg/kg | High-fat diet-fed adult male Wistar rats | Normalized GSH content in the RK-treated group, compared with that in the high-fat diet group | [66] | ||
| MDA↓ | 0.5%, 1% or 2% | High-fat diet-fed male female Sprague-Dawley rats | MDA level in RK high-dose group (36.2798 ± 6.454 nmol/mg of protein) was significantly lower than that in the high-fat diet group (47.9707 ± 3.187 nmol/mg of protein) | [56] | |
| 44 mg/kg | High-fat diet-fed male Wistar albino rats | Decreased MDA level in RK-treated group (29 ± 4.2 m/dL compared with that in the obese group (48.1 ± 5.2 mg/dL) | [61] | ||
| 50, 100 and 200 mg/kg | Wistar albino rats induced myocardial by ISO | Significant reductions in MDA level in medium- and high-dose of RK groups (5.84 ± 0.33 and 5.66 ± 0.34 nmol MDA/mg protein, respectively) compared with that in the ISO-treated group (9.40 ± 0.45 nmol MDA/ mg protein) | [62] | ||
| 6 mg/kg | Male albino rats induced toxicity by AA | RK co-treatment ameliorated the MDA level (13.18 ± 2.618 nmol/mL) compared with that in AA-treated group (20.83 ± 1.81 nmol/mL) | [63] | ||
| 25, 50, 100 and 200 mg/kg | Adult male Swiss albino rats induced pulmonary toxicity by CP | Dose-dependent recovery of MDA level (537.04 ± 13.73, 456.79 ± 5.12, 424.69 ± 6.67 and 374.07 ± 5.32 U/mg protein, respectively) by RK pre-treatment against CP-induced toxicity (730.25 ± 16.07 nmol/mg protein) | [64] | ||
| 250 and 500 mg/kg | High-fat diet-fed Male Wistar albino rats | RK treatment reduced MDA by approximately 50% compared with that in the obese group | [65] | ||
| 55 mg/kg | High-fat diet-fed adult male Wistar rats | RK treatment group normalized the MDA level | [66] | ||
| Nrf-2 ↑ | 50 mg/kg | Adult male Wistar rats induced gastric lesion by EtOH | Nrf-2 expression in the RK-treated group was increased by 50% compared with that in the EtOH-treated group | [54] | |
| NOXs ↓ | 50 mg/kg | Adult male Wistar rats induced gastric lesion by EtOH | NOX-1 and NOX-4 expressions in the RK-treated group were abated by about 50% compared with that in the EtOH-treated group | [54] | |
AA, acrylamide; CAT, catalase; CCl4, carbon tetrachloride; CP, cyclophosphamide; EtOH, ethanol; GSH, glutathione; GSH-Px, glutathione peroxidase; H2O2, hydrogen peroxide; ISO, isoproterenol; MDA, malondialdehyde; NOXs, NADPH oxidases; Nrf-2, nuclear factor erythroid-derived 2-related factor 2; SOD, superoxide dismutase; TAC, total antioxidant capacity. The up arrow (↑) means that the level or expression of each variable has increased, and the down arrow (↓) indicates the decrease in the corresponding value.