Salehi I, Mohammadi M, Mirzaei F, Soufi F G
Department of Physiology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Cardiovasc J Afr. 2012 Feb;23(1):18-22. doi: 10.5830/CVJA-2010-091.
Oxidative stress is a key component of atherosclerosis. It has been suggested that amlodipine inhibits oxidative stress. In this study, we evaluated the effects of amlodipine on the total antioxidant capacity of heart tissue and blood in 36 control and cholesterol-fed male New Zealand white rabbits.
The rabbits were divided into four groups (n = 9). Group 1 rabbits were fed a regular diet, group 2 were fed a diet with 2% cholesterol, group 3 were fed a regular diet plus 5 mg/kg/day oral amlodipine, and group 4 were fed 2% cholesterol diet plus amlodipine 5 mg/kg/day. At the end of eight weeks, blood samples were drawn and at the same time heart tissue was isolated and frozen in liquid nitrogen. After homogenisation, the solution was centrifuged and the light supernatant was stored at -80°C. This was used for determination of glutathione peroxidase (GPX), superoxide dismutase (SOD) and (MDA) levels.
Eight weeks of amlodipine treatment significantly reduced the levels of total cholesterol, low-density lipoprotein cholesterol and triglycerides in the group on the hypercholesterolaemic diet (p < 0.05). In the blood, the level of thiobarbituric acid-reactive substances increased in the rabbits on the 2% cholesterol diet (group 2) and 2% cholesterol-plusamlodipine diet (group 4) and decreased in the amlodipineonly group (group 3) (p < 0.05). Lipid peroxidation in the heart tissue was similar to that in the blood, except in the amlodipine-only group (group 3). In the blood, the activity of total SOD (tSOD) decreased in the group on the 2% cholesterol diet (group 2) (p < 0.05) and markedly increased in the amlodipine-only (group 3) and 2% cholesterol-plusamlodipine groups (group 4) (p < 0.05).
Amlodipine decreased oxidative stress in the heart and blood and improved the lipid profile in cholesterolfed rabbits. Therefore, it may be considered a useful tool for the reduction of oxidative stress and improvement of lipid profiles in diseases related to atherosclerosis.
氧化应激是动脉粥样硬化的关键组成部分。有人提出氨氯地平可抑制氧化应激。在本研究中，我们评估了氨氯地平对36只对照和喂食胆固醇的雄性新西兰白兔心脏组织和血液总抗氧化能力的影响。
将兔子分为四组（n = 9）。第1组兔子喂食常规饮食，第2组喂食含2%胆固醇的饮食，第3组喂食常规饮食加5毫克/千克/天口服氨氯地平，第4组喂食含2%胆固醇的饮食加5毫克/千克/天氨氯地平。在八周结束时，采集血样，同时分离心脏组织并在液氮中冷冻。匀浆后，将溶液离心，上清液储存在-80°C。用于测定谷胱甘肽过氧化物酶（GPX）、超氧化物歧化酶（SOD）和丙二醛（MDA）水平。
八周的氨氯地平治疗显著降低了高胆固醇饮食组的总胆固醇、低密度脂蛋白胆固醇和甘油三酯水平（p < 0.05）。在血液中，2%胆固醇饮食组（第2组）和2%胆固醇加氨氯地平饮食组（第4组）的硫代巴比妥酸反应性物质水平升高，而仅氨氯地平组（第3组）降低（p < 0.05）。心脏组织中的脂质过氧化与血液中的相似，但仅氨氯地平组（第3组）除外。在血液中，2%胆固醇饮食组（第2组）的总SOD（tSOD）活性降低（p < 0.05），而仅氨氯地平组（第3组）和2%胆固醇加氨氯地平组（第4组）显著升高（p < 0.05）。
氨氯地平降低了心脏和血液中的氧化应激，并改善了喂食胆固醇兔子的血脂谱。因此，它可能被认为是减少氧化应激和改善与动脉粥样硬化相关疾病血脂谱的有用工具。
