Ozer Nesrin Kartal, Negis Yesim, Aytan Nurgül, Villacorta Luis, Ricciarelli Roberta, Zingg Jean-Marc, Azzi Angelo
Department of Biochemistry, Faculty of Medicine, Marmara University, 34668 Haydarpasa, Istanbul, Turkey.
Atherosclerosis. 2006 Jan;184(1):15-20. doi: 10.1016/j.atherosclerosis.2005.03.050. Epub 2005 Jun 23.
A numerous studies suggest that Vitamin E has a preventive role in atherosclerosis, although the mechanism of action still remains unclear. CD36, a member of the scavenger receptor family is centrally involved in the uptake of oxidized low density proteins (oxLDLs) from bloodstream. During the atherosclerotic process, the lipid cargo of oxLDL accumulates in macrophages and smooth muscle cells, inducing their pathological conversion to foam cells. In the present study, we investigate the role of Vitamin E on CD36 expression in an in vivo model. Atherosclerosis was induced by a 2% cholesterol containing Vitamin E poor diet. Three groups of six rabbits each were studied. The first group (control) was fed on Vitamin E poor diet. The second group was fed with Vitamin E poor diet containing 2% cholesterol and the rabbits in the third group were fed with Vitamin E poor diet containing 2% cholesterol and received injections of 50 mg/kg of Vitamin E i.m. After 4 weeks, aortas were removed and analysed by light microscopy for atherosclerotic lesions. Aortic samples were analysed for CD36 mRNA expression. The aortas of cholesterol-fed rabbits showed typical atherosclerotic lesions, detected by macroscopic and microscopic examination, and exhibited an increase in CD36 mRNA expression. Vitamin E fully prevented cholesterol induced atherosclerotic lesions and the induction of CD36 mRNA expression. The effects observed at the level of CD36 scavenger receptor expression in vivo suggest an involvement of reduced foam cell formation in the protective effect of Vitamin E against atherosclerosis.
大量研究表明维生素E在动脉粥样硬化中具有预防作用，尽管其作用机制仍不清楚。CD36是清道夫受体家族的一员，在从血液中摄取氧化型低密度脂蛋白（oxLDL）过程中起核心作用。在动脉粥样硬化过程中，oxLDL的脂质成分在巨噬细胞和平滑肌细胞中积累，诱导它们病理性转化为泡沫细胞。在本研究中，我们在体内模型中研究了维生素E对CD36表达的作用。通过含2%胆固醇且缺乏维生素E的饮食诱导动脉粥样硬化。研究了三组，每组六只兔子。第一组（对照组）喂食缺乏维生素E的饮食。第二组喂食含2%胆固醇且缺乏维生素E的饮食，第三组兔子喂食含2%胆固醇且缺乏维生素E的饮食，并接受50mg/kg维生素E的肌肉注射。4周后，取出主动脉，通过光学显微镜分析动脉粥样硬化病变。分析主动脉样本中CD36 mRNA的表达。喂食胆固醇的兔子的主动脉显示出典型的动脉粥样硬化病变，通过宏观和微观检查检测到，并表现出CD36 mRNA表达增加。维生素E完全预防了胆固醇诱导的动脉粥样硬化病变以及CD36 mRNA表达的诱导。在体内CD36清道夫受体表达水平观察到的效应表明，减少泡沫细胞形成参与了维生素E对动脉粥样硬化的保护作用。
