TABLE 3.
Effect of naringin and naringenin on hypertension and cardiac function in animal and human studies1
| Derivative and dose | Model | Experimental outcome | Reference |
| Hypertension | |||
| Naringin | |||
| 100 mg · kg bw−1 · d−1 | High-fat/high-carbohydrate–fed Wister rats | Decreased blood pressure | (64) |
| Improved endothelial dysfunction, probably by increasing bioavailability of NO | |||
| 250, 500, and 1000 mg/kg diet | Stroke-prone hypertensive rats | Decreased blood pressure, probably by increasing bioavailability of NO | (65) |
| Naringenin | |||
| 10 mg · kg bw−1 · d−1 | Streptozotocin-induced diabetic rats | Endothelium-dependent relaxation to acetylcholine was significantly higher in naringenin-treated diabetic rats | (66) |
| — | VSMC proliferation and migration | Naringenin inhibited TNF-α–induced VSMC proliferation and migration in a dose-dependent manner | (68) |
| Prevented ERK/MAPK and Akt phosphorylation and left p38 MAPK and JNK unchanged | |||
| HO-1 is involved | |||
| Naringin (with narirutin) | |||
| 0.5 L/d (677 mg/L naringin) | In patients with stage I hypertension | Sweetie juice was shown to have a significant beneficial effect in reducing diastolic blood pressure | (69) |
| Cardiac function | |||
| Naringin | |||
| 100 mg · kg bw−1 · d−1 | High-fat/high-carbohydrate–fed Wister rats | Decreased inflammatory cell infiltration and fibrosis | (64) |
| Decreased left ventricular stiffness and improved echocardiographic variables such as fractional shortening, ejection fraction, left ventricular internal diameter in diastole, etc. | |||
| 10, 20, and 40 mg/kg bw, respectively | Isoproterenol-induced myocardial infarction in rats | Significantly decreased the concentrations of lipid peroxidative products and improved antioxidant status by increasing the activities of antioxidant enzymes and nonenzymatic antioxidants | (70) |
| 10 mg/kg bw | Doxorubicin-induced cardiotoxicity in mice | Prior exposure of mice to naringin before doxorubicin administration significantly reduced serum concentrations of AST, ALT, CK-MB, and LDH, indicating that naringin protected against doxorubicin-induced cardiotoxicity | (71) |
| 10, 20, and 40 mg/kg | Isoproterenol-induced myocardial infarction in Wistar rats | Restored the normal mitochondrial function. | (72) |
| Transmission electron microscopic observations confirmed the protection of mitochondrial architecture | |||
| Naringenin | |||
| 10−4–10−5 mol/L | H9c2 cardiomyocyte cells | Naringenin inhibited daunorubicin apoptosis of H9c2 cardiomyocytes cells in vitro | (73) |
1
Akt, protein kinase B; ALT, alanine transaminase; AST, aspartate transaminase; bw, body weight; CK-MB, creatine kinase-MB; ERK, extracellular signal–regulated kinase; HO-1, heme oxygenase 1; JNK, c-Jun N-terminal kinase; LDH, lactate dehydrogenase; MAPK, mitogen-activated protein kinase; NO, nitric oxide; VSMC, vascular smooth muscle cell.