Steinberg D
University of California, San Diego, Department of Medicine, La Jolla 92093-0682, USA.
Lancet. 1995 Jul 1;346(8966):36-8. doi: 10.1016/s0140-6736(95)92657-7.
The hypothesis that oxidative modification of low density lipoprotein contributes to the progression of atherosclerosis is supported by an impressive body of in-vitro findings and by persuasive results in animal models of atherosclerosis. The hypothesis was originally proposed specifically to account for foam cell formation but oxidation of LDL has now been shown to confer on it a long list of new biological properties any one of which could in principle enhance its atherogenicity. The relative importance of these altered biological properties in vivo remains uncertain. Whatever the precise mechanisms, we know that antioxidants can slow the atherogenic process in several experimental models, including LDL-receptor-deficient rabbits, cholesterol-fed rabbits, and cholesterol-fed non-human primates. Of 18 published studies, 13 have given strongly positive results, the rate of progression of lesions being reduced by 50-80%; 2 have yielded marginally positive results; and 3 have been negative (see ref 3 for references). Furthermore, the fact that four different antioxidant compounds have been used--probucol, butylated hydroxytoluene, N,N'-diphenyl-phenylenediamine, and vitamin E--supports the conclusion that they are working via the property they all share, namely, their antioxidant potential.
低密度脂蛋白的氧化修饰会促进动脉粥样硬化进展这一假说，得到了大量体外研究结果以及动脉粥样硬化动物模型中具有说服力的结果的支持。该假说最初是专门为解释泡沫细胞形成而提出的，但现在已表明，低密度脂蛋白的氧化赋予了它一系列新的生物学特性，其中任何一种特性原则上都可能增强其致动脉粥样硬化性。这些改变的生物学特性在体内的相对重要性仍不确定。无论确切机制如何，我们知道抗氧化剂可以在几种实验模型中减缓动脉粥样硬化进程，包括低密度脂蛋白受体缺陷型兔子、喂食胆固醇的兔子以及喂食胆固醇的非人类灵长类动物。在已发表的18项研究中，13项给出了强烈的阳性结果，病变进展速率降低了50%至80%；2项得出了勉强算是阳性的结果；3项为阴性结果（参考文献见参考文献3）。此外，使用了四种不同的抗氧化化合物——普罗布考、丁基羟基甲苯、N,N'-二苯基对苯二胺和维生素E——这一事实支持了它们通过其共有的特性（即抗氧化潜力）发挥作用的结论。
