Effect of vitamin E on aortic lipid oxidation and intimal proliferation after arterial injury in cholesterol-fed rabbits.
Effect of vitamin E on aortic lipid oxidation and intimal proliferation after arterial injury in cholesterol-fed rabbits.
复制标题
维生素 E 对胆固醇喂养兔动脉损伤后主动脉脂质氧化和内膜增殖的影响。
DOI：
10.1016/s0891-5849(01)00721-3
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发表时间：
2001
影响因子：
7.4
通讯作者：
KeaneyJr,JF
中科院分区：
文献类型：
--
作者：
Upston,JM;Witting,PK;Brown,AJ;Stocker,R;KeaneyJr,JF
氧化低密度脂蛋白（LDL）与动脉粥样硬化有关。然而，旨在测试维生素 E 等抗氧化剂是否可以改善心血管疾病的大规模干预研究却产生了矛盾的结果。这可能与体内引发脂质氧化的机制尚不清楚以及缺乏动脉粥样硬化病变中抗氧化剂缺乏的直接证据有关。此外，几乎没有证据表明维生素 E 作为体内脂质过氧化的抗氧化剂。在这里，我们测试了膳食维生素 E（α-生育酚）补充剂对球囊损伤、高胆固醇血症兔子的内膜增殖和脂质氧化的抗氧化作用。与未补充和缺乏 α-生育酚的食物相比，补充 α-生育酚可使血管中 α-生育酚的含量增加 30 倍以上。球囊损伤导致主动脉氧化脂质沉积。以酯化脂质 (LOOH) 和氧化亚油酸酯 (HODE) 的氢过氧化物测量，初级脂质氧化产物的最大水平为 0.22 和 1.10 nmol/mg，分别占前体分子的 0.21 和 0.39%。以氧固醇测量的次级脂质氧化产物最大为 5.60 nmol/mg 或前体化合物的 1.48%。补充维生素E可显着降低血管HODE和氧甾醇。然而，主动脉血管的内膜/中膜比率随着维生素E的补充而增加，这表明抗氧化剂促进了内膜增殖。因此，该研究证明了主动脉脂质氧化与病变发展之间的分离，并表明维生素 E 不会阻止该动物模型中的病变发展。
Oxidized low-density lipoproteins (LDL) are implicated in atherosclerosis. However, large-scale intervention studies designed to test whether antioxidants, such as vitamin E, can ameliorate cardiovascular disease have generated ambivalent results. This may relate to the fact that the mechanism whereby lipid oxidation is initiated in vivo is unknown and the lack of direct evidence for a deficiency of antioxidants in atherosclerotic lesions. Further, there is little evidence to suggest that vitamin E acts as an antioxidant for lipid peroxidation in vivo. Here we tested the antioxidant effect of dietary vitamin E (α-tocopherol) supplementation on intimal proliferation and lipid oxidation in balloon-injured, hypercholesterolemic rabbits. α-Tocopherol supplementation increased vascular content of α-tocopherol over 30-fold compared to nonsupplemented and α-tocopherol-deficient chows. Balloon injury resulted in oxidized lipid deposition in the aorta. Maximum levels of primary lipid oxidation products, measured as hydroperoxides of esterified lipid (LOOH) and oxidized linoleate (HODE), were 0.22 and 1.10 nmol/mg, representing 0.21 and 0.39% of the precursor molecule, respectively. Secondary lipid oxidation products, measured as oxysterols, were maximal at 5.60 nmol/mg or 1.48% of the precursor compound. Vascular HODE and oxysterols were significantly reduced by vitamin E supplementation. However, the intima/media ratio of aortic vessels increased with vitamin E supplementation, suggesting that the antioxidant promoted intimal proliferation. Thus, the study demonstrates a dissociation of aortic lipid oxidation and lesion development, and suggests that vitamin E does not prevent lesion development in this animal model.