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为探讨葡萄籽提取物抗实验性动脉粥样硬化作用及机理 ,将 5 0只动脉粥样硬化敏感株近交系C5 7BL 6J小鼠 ,随机分为正常对照组、高脂模型组、葡萄籽提取物低、高剂量组和药物对照组 ,正常对照组和高脂模型组 ,每日分别给予普通饲料和高脂饲料 ,葡萄籽提取物组和药物对照组 ,在每日给予高脂饲料的同时 ,分别添加葡萄籽提取物 (0 2mg g、0 6mg g体重 )和普托罗考片 (0 2mg g体重 ) ,实验至第 2 1周末 ,眼球放血处死小鼠 ,检测血清氧化型低密度脂蛋白 (OX LDL)、细胞粘附因子 1(ICAM 1)和一氧化氮 (NO)含量 ,同时取主动脉作病理形态学观察。结果发现 ,葡萄籽提取物组 ,血清OX LDL和ICAM 1水平均高于正常对照组 ,但明显低于高脂模型组 ,血清NO水平 ,则低于正常对照组而高于高脂模型组。观察主动脉部位的形态显示 ,葡萄籽提取物组其血管壁增厚程度、玻璃样改变和泡沫细胞数量均轻于模型组 ,高剂量组效果为佳 ,但仍重于正常对照组。实验结果提示 ,葡萄籽提取物具有减缓C5 7BL 6J小鼠动脉粥样硬化形成的作用 ,这可能与阻抑OX LDL、ICAM 1含量升高减低对血管内皮细胞损伤及保护血管内皮功能等作用有关
In order to investigate the anti-atherosclerotic effect and mechanism of grape seed extract, 50 atherosclerotic susceptible strains of inbred strain C5 7BL 6J were randomly divided into normal control group, high fat model group, grape seed Low-dose, high-dose group and drug control group, normal control group and high-fat model group were given daily feed and high-fat diet, grape seed extract group and drug control group, given daily high-fat diet At the same time, grape seed extract (0 2 mg g, 0 6 mg g body weight) and pinotrope test (0 2 mg g body weight) were added respectively. At the end of the 21st week, mice were sacrificed by exsanguination. OX LDL, ICAM 1 and NO, and the aorta was taken for histopathological observation. The results showed that the levels of serum OX LDL and ICAM 1 in grape seed extract group were higher than those in normal control group, but significantly lower than those in high-fat model group and serum NO group, which were lower than those in normal control group and high-fat model group. The morphological changes of the aorta showed that the extent of vascular wall thickening, the change of the vitreous and the number of the foam cells in the grape seed extract group were all lower than those in the model group. The effect of the high dose group was better than that of the normal control group. The experimental results suggest that grape seed extract can slow down the formation of atherosclerosis in C5 7BL 6J mice, which may be related to the inhibition of the increase of OX LDL and ICAM 1, the decrease of vascular endothelial cell damage and the protection of vascular endothelial function