Jacobsson Leif S, Yuan Xi Ming, Ziedén Bo, Olsson Anders G
Department of Pharmacology, Faculty of Health Sciences, Linköping University, Linköping SE-581 85, Sweden.
Atherosclerosis. 2004 Apr;173(2):231-7. doi: 10.1016/j.atherosclerosis.2004.01.003.
The aim of this study was to evaluate the influence of -tocopherol and astaxanthin on low-density lipoprotein (LDL) oxidation lag time and atherosclerotic lesion formation in Watanabe heritable hyperlipidemic (WHHL) rabbits. Thirty-one, 3-month-old WHHL rabbits were divided into three experimental groups. One group (n=10) was fed standard rabbit feed alone and served as a control, a second group (n=11) was supplied with the same feed containing 500 mg alpha-tocopherol/kg and a third group (n=10) was given a feed containing 100 mg astaxanthin/kg. Plasma lipids, lipoproteins and LDL oxidation lag time were followed for 24 weeks. At the end of the treatment period, the animals were killed and the thoracic aorta was used for evaluation of the degree of atherosclerosis. Colour photographs of the intimal surface of the vessel were taken for determination of the atherosclerotic area. Cross-sections of the thoracic aorta were used for histological examination and for determination of intimal thickening. Specimens of the vessel were used for determination of the tissue cholesterol content. Plasma cholesterol remained at a high level during the time of the experiment and there were no differences between the experimental groups. After 24 weeks, the LDL oxidation lag time was 53.7+/-1.7 min, 109+/-4 min (P<0.001) and 56.4+/-3.4 min (P=0.47) in the control, alpha-tocopherol and astaxanthin groups, respectively. In the thoracic aorta, the atherosclerotic area was 80.7+/-5.1%, 67.1+/-6.7% (P=0.13) and 75.2+/-5.7% (P=0.49) in the control, alpha-tocopherol and astaxanthin groups, respectively. The intimal thickening was 45.6+/-3.2%, 44.0+/-4.1% (P=0.89) and 40.0+/-4.5% (P=0.33) in the control, alpha-tocopherol and astaxanthin groups, respectively. Finally, the cholesterol content was 107+/-9 mol/g, 95.7+/-11.5 mol/g (P=0.31) and 101+/-5 mol/g (P=0.33) in the control, alpha-tocopherol and astaxanthin groups, respectively. It can be concluded that alpha-tocopherol but not astaxanthin prolonged the LDL oxidation lag time. The two antioxidative substances did not prevent atherogenesis in WHHL rabbits in this setting.
本研究的目的是评估生育酚和虾青素对渡边遗传性高脂血症(WHHL)兔低密度脂蛋白(LDL)氧化延迟时间和动脉粥样硬化病变形成的影响。31只3月龄的WHHL兔被分为三个实验组。一组(n = 10)仅喂食标准兔饲料作为对照,第二组(n = 11)喂食含500 mgα-生育酚/kg的相同饲料,第三组(n = 10)喂食含100 mg虾青素/kg的饲料。连续24周监测血浆脂质、脂蛋白和LDL氧化延迟时间。在治疗期结束时,处死动物,取胸主动脉评估动脉粥样硬化程度。拍摄血管内膜表面的彩色照片以确定动脉粥样硬化面积。取胸主动脉横截面进行组织学检查并测定内膜增厚情况。取血管标本测定组织胆固醇含量。实验期间血浆胆固醇水平一直很高,各实验组之间无差异。24周后,对照组、α-生育酚组和虾青素组的LDL氧化延迟时间分别为53.7±1.7分钟、109±4分钟(P<0.001)和56.4±3.4分钟(P = 0.47)。在胸主动脉中,对照组、α-生育酚组和虾青素组的动脉粥样硬化面积分别为80.7±5.1%、67.1±6.7%(P = 0.13)和75.2±5.7%(P = 0.49)。内膜增厚情况在对照组、α-生育酚组和虾青素组分别为45.6±3.2%、44.0±4.1%(P = 0.89)和40.0±4.5%(P = 0.33)。最后,对照组、α-生育酚组和虾青素组的胆固醇含量分别为107±9 μmol/g、95.7±11.5 μmol/g(P = 0.31)和101±5 μmol/g(P = 0.33)。可以得出结论,生育酚而非虾青素延长了LDL氧化延迟时间。在这种情况下,这两种抗氧化物质并未预防WHHL兔的动脉粥样硬化形成。