| Type of study model | Experimental method [subject (age/weight), treatment dosage, duration of treatment] | Major activity | Mechanism of action | Reference |
| In vivo study | HCD ICR mice (7 weeks), reverse osmosis-DSW 44.6 hardness, Electrodialysis-DSW 4685.9 hardness, 10% DSW 544.2 hardness, 8 weeks | Reduced abnormal cardiac architecture, apoptosis in left ventricle (LV). Increased cardiac survival signalling components in LV of mice. Change in Fas and mitochondrial-dependent apoptotic components in LV of mice. Change in apoptosis related proteins and cardiac apoptotic cells in LV of mice. | Decreased LV diameter, LV thickness, and ratio of thickness to diameter in hearts. Increased insulin-like growth factor-1 receptor, phosphoinositide-3-kinases, and p-AKT/AKT ratio. Decreased the protein products of TNF-α in LV of mice. Decreased levels of Fas, cytochrome c, cleaved caspase-9, t-Bid, and cleaved caspase-3. Decreased Bak and increased antiapoptotic proteins, including Bcl-XL and ratio of p-Bad to Bad. Decreased TUNEL-positive cardiac cells. | [25] |
| In vivo study | High fat/cholesterol-fed (HFCD) male Syrian Golden hamster (5 weeks), DSW 300, 900, and 1500 hardness, ad libitum, 6 weeks | Decreased levels of serum TC, TG, atherogenic index, and malondialdehyde.
| Increase in daily faecal lipid of TG and TC and bile acid outputs. Upregulated hepatic low-density-lipoprotein receptor (LDL receptor) and cholesterol-7a-hydroxylase (CYP7A1) gene expressions. Increase of serum trolox equivalent antioxidant capacity (TEAC). | [5] |
| In vivo study | Kurosawa and Kusanagi-Hypercholesterolemic (KHC) rabbits (4 months), DSW 1000 hardness, 500 ml/d, 6 months | Improved cardiovascular hemodynamics. | Lowered systolic, diastolic pulse, mean arterial pressures, and total peripheral resistance. | [2] |
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