Table 1.
Animal investigations of astaxanthin effects related to the cardiovascular system.
| Study | Model | Dose | Duration/timing of supplementation | Effects of (metabolized) astaxanthin |
|---|---|---|---|---|
| Lauver et al. 2008 [38] | Dog (occlusive carotid artery thrombus) | IV DDA 10, 30, or 50 mg/kg/body weight | 30 mins after occlusion | - Reduced incidence of secondary thrombosis |
| Aoi et al. 2003 [61] | C57BL/6 mice | Diet supplemented with astaxanthin 0.02% weight/weight and food intake recorded | 3 weeks | - Attenuation of exercise increased 4-hydroxy-2-nonenal-modified protein and 8-hydroxy-2′-deoxyguanosine in cardiac and gastrocnemius muscle |
| - Attenuation of exercise increases in creatine kinase and myeloperoxidase activity in cardiac and gastrocnemius muscle | ||||
| - Astaxanthin accumulated in cardiac and gastrocnemius muscle | ||||
| Gross and Lockwood 2004 [39] | Myocardial infarct model Sprague-Dawley rats | DDA 25/50/75 mg/kg intravenously daily | 4 days prior to myocardial infarction | - Myocardial infarct size significantly reduced |
| Li et al 2004 [70] | WHHL rabbits | 100 mg astaxanthin/kg feed | 24 weeks | Reduced macrophage infiltration into plaque, improved plaque stability and decreased apoptosis |
| Hussein et al. 2005 [75] | Stroke prone Spontaneously hypertensive rats | 50 mg/kg body weight/day | 5 weeks | - Significant blood pressure reduction |
| - Delayed incidence of stroke | ||||
| Lauver et al. 2005 [76] | Rabbit model of myocardial ischemia/reperfusion | DDA 50 mg/kg/day intravenously | 5 days | - Significant reduction in complement activation |
| - Significant reduction in myocardial infarct size | ||||
| Gross et al. 2005 [74] | Canine model of myocardial ischemia/reperfusion | DDA 50 mg/kg/day intravenously | 2 h or daily for 4 days | - Significant reduction in myocardial infarct size |
| - Two of three dogs treated for four days had 100% cardiac protection | ||||
| Gross et al. 2006 [40] | Sprague-Dawley rats Left anterior descending coronary artery occlusion/reperfusion | DDA 125 or 500 mg/kg/day orally | 7 days | - Astaxanthin loading of myocardium indicating good bioavailability |
| - Trends in lowering of lipid peroxidation products | ||||
| - Significant reduction in myocardial infarct size | ||||
| Hussein et al. 2006 [77] | Spontaneously hypertensive rats | 5 mg/kg body weight/day | 7 days | - Significant reduction in nitric oxide end products |
| - Significant reduction in elastin bands in aorta | ||||
| - Significant reduction in wall/lumen arterial ratio in coronary arteries | ||||
| Hussein et al 2006 [71] | SHR/NDmcr- cp rats | Astaxanthin 50 mg/kg/d | 22 weeks | Astaxanthin significantly reduced BP, fasting BSL, insulin resistance and sensitivity, triglyceride and non-esterified fatty acid levels. Astaxanthin decreased fat cell size |
| Kishimoto et al 2009 [69] | Human monocytic cell line THP-1 | Astaxanthin 5–10 μM | 24 h | Astaxanthin inhibits activation of macrophages |
| Nakao et al. 2010 [78] | BALC/c mice | Astaxanthin 0, 0.02, 0.08% orally/day | 8 weeks | - No change in blood glutathione concentration |
| - No change in lymphocyte mitochondrial membrane potential | ||||
| - Higher myocardial mitochondrial membrane potential and contractility index | ||||
| Khan et al. 2010 [54] | C57BL/6 mice | CDX-085 500 mg/kg/d | 14 days | - Free astaxanthin present in the plasma, heart, liver and platelets |
| - Significantly increased basal arterial blood flow and delay in occlusive thrombosis after endothelial injury | ||||
| Human umbilical vein endotheilial cells and platelets from Wistar-Kyoto rats | - Significantly increased release of nitric oxide and decreased peroxynitrite levels | |||
| Aduri et al. 2011 [79] | Rat | VitaePro 70 mg/kg BW (Containing astaxanthin 2%) | 21 days | - Significantly reduced myocardial infarct size |
| - Significantly reduced apoptosis and oxidative stress |
VitaePro-astaxanthin zeaxanthin and luetin. WHHL-Watanabe heritable hyperlipidemic rabbits.