|
| Study Design | Doses | Route of administration | Effects | Ref |
|
| H9c2 embryonic rat cardiac cells | (0, 50, 100, 150, 200) μmol/L | Expose | ↓CoCl2-induced cell death
↓HIF-1α expression
↓CoCl2-induced apoptosis
↑Bcl-2/Bax ratio | [18] |
|
| Human umbilical cord blood (HUCB) | 1010–10−5 μmol | Expose | ↑ECFCs' proliferation and migration
↑Expression of α-parvin, F-actin, ILK
↑Phosphorylation of the signaling of ERK 1/2
↑ECFCs (GS-ECFCs)
↑Proliferation of the Cells
↑Angiogenic cytokines
↑Neovascularization
↓Myocardial fibrosis
↑Cardiac function
↑Regenerative potential in ischemic tissues | [19] |
|
| H9c2 cardiomyoblast cells | 10−10–10−5 M | Expose | ↓Caspase-3, caspase-8, caspase-9, and Bad
↑Phosphor (p)-Akt, p-Erk1/2, and p-Bad.
↑Erk1/2, Akt, and NF κ B proteins | [20] |
|
| H9c2 cells | 10 µM | Expose | ↓Damage of H9c2 cells
↑Cells growth ability
↓Apoptosis
↓Inflammatory response
↓Myc expression
↓P-P38 MAPK and p-JNK expression | [21] |
|
| Cardiomyoblasts (H9C2) | 10 Pm–100 nM | Expose | ↑Endothelial NOS‑dependent NO by the modulation of intracellular signaling related to p38MAPK, ERK1/2, and Akt | [22] |
|
| Human Heart cells | 5 mg/kg | Expose | ↓PICR and P/Ht
↑Dysfunction
↓MNCX
↑MKATP channels | [23] |
|
| Cultured cardiac fibroblasts (CFs) | 10,50,100 μM | Expose | ↓TGFβ1-induced proliferation
↓production of collagen
↓Myofibroblast transformation
↓TGFβ-activated kinase 1 (TAK1)
↑Antifibrotic effects | [27] |
|
| Culture of ventricular myocytes from neonatal rats | 70 μM | Expose | ↓ANF
↓Fos
↓MLC-2
↓(MAP) kinases
↓GTP | [28] |
|
| Rats | 250 mg/kg | Injected once daily for 2 days | ↑Contractility
↑Cardiac output
↑Ischemic tolerance
↑Mean (SEM) recovery of contractility and cardiac output
↓Mean glucose transporter protein 4 | [24] |
|
| Rats | 0.1, 0.2 mg/kg | Subcutaneous injection | ↓Heart weight to body weight ratio
↓Left ventricular mass
↓1-OH proline and oxidative stress ↓ Myocardial fibrosis | [25] |
|
| Rats | 5 mg/kg or 3 mg/kg | Intraperitoneal | ↑SR Ca leak
↑Diastolic contracture | [26] |
|
| C57/BL6 mice | 40 mg/kg/day for 7 weeks | Gavage | ↑Cross-sectional area of cardiomyocytes
↓AKT/GSK-3β signaling and MAPK (JNK1/2, P38, and ERK1/2)
↑Collagen volume fraction
↑ANP
↓BNP
↑β-MHC
↓CTGF
↓Fibronectin, collagen Iα, collagen III
↓TGF-β1
↓Vimentin mRNA
↓MAPK (JNK1/2, P38, and ERK1/2) | [37] |
|
| Rats | 1 mg/kg/day | Injection | ↓Right ventricular
↓PH-induced pulmonary vascular | [30] |
|
| Pigs | 0.075 mg/min | Infused | ↑Coronary blood flow
↑Phosphorylation of NO synthase
↑NO production through p38 MAPK, ERK 1/2, and Akt pathways
↑Coronary vasodilation
↑Release of NO | [31] |
|
| Rats | (0.25, 0.5, 1.0, 1.5, 3, and 5 mg kg) | I.V., 5 min after coronary artery occlusion | ↓Necrosis of myocardia
↓MPO activity
↓Serum CPK activity
↑Myocardial contractility
↓Ventricular arrhythmias
↓TNF-alpha and blunted ICAM-1
↓Inflammatory response | [32] |
|
| In 22 postmenopausal patients | 54 mg/day | One-year genistein dietary supplementation | ↑LA area fractional change
↑LV ejection fraction
↑LA remodeling | [33] |
|
| Human | — | Dietary intake | ↓NF-kappa B
↓Akt signaling
↓Direct antioxidant action
↓Estrogen and androgen-mediated molecular pathways | [34] |
|
| Rabbits | 0.2 mg/kg/day | Subcutaneously | A single dose of genistein had no protective effect | [35] |
|
| Mice | 600 mg/kg | Were fed | ↑Echocardiographic changes in function
↑LVID
↑Whole heart surface area
↑Cardiac GLUT4 protein expression
↑GLUT4 protein expression | [36] |
|
