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apoA—Ⅰ、apoC-Ⅲ基因限制性片段长度多态性(RFLP)与动脉粥样硬化(AS)的关系研究,无疑是从基因水平直接探讨 AS 发病机理的本质。本文介绍了近几年来这方面研究的状况。研究发现,apoA-Ⅰ基因的Pst-Ⅰ 3.2Kb 片段不仅与家族性低α-脂蛋白血症有关,而且在冠心病患者中出现的频率约为正常人8倍之高。此外,apoA-Ⅰ基因的 EcoRⅠ 6.5Kb片段,在冠心病发生心肌梗塞的患者中出现的频率也很高,暗示这种 RFLP 还可能与 AS 的严重程度有一定关。apoC-Ⅲ基因 RFLP 与 AS 的关系研究提示,apoC-Ⅲ基因的 Sst-Ⅰ 3.2Kb 片段除与高甘油三酯血症相关联外,在高胆固醇血症以及心肌梗塞患者中所出现的频率亦明显高于正常人。值得提及的是,Kavatha-nasis 等所发现的 apoA-Ⅰ、apoC-Ⅲ联合缺乏的患者,其过早发生 AS 与 apoA-Ⅰ基因和 aPOC-Ⅲ基因发生重组有关。
ApoA-Ⅰ, apoC-Ⅲ gene restriction fragment length polymorphism (RFLP) and atherosclerosis (AS) study, no doubt directly from the gene level explore the nature of the pathogenesis of AS. This article describes the status of research in this area in recent years. The study found that apoA-Ⅰ gene Pst-Ⅰ 3.2Kb fragment not only with familial hypoalphalipoproteinemia, but also in patients with coronary heart disease frequency of about 8 times the normal high. In addition, apoA-Ⅰ gene EcoRⅠ 6.5Kb fragment in patients with myocardial infarction in coronary heart disease also appeared in high frequency, suggesting that this RFLP may also have a certain degree of severity of AS. ApoC-Ⅲ gene RFLP and AS relationship studies suggest that, apoC-Ⅲ gene Sst-Ⅰ 3.2Kb fragment in addition to hypertriglyceridemia associated with hypercholesterolemia and myocardial infarction in patients with frequency also Obviously higher than normal people. It is worth mentioning that premature AS in patients with apoA-Ⅰ and apoC-Ⅲ deficiency discovered by Kavatha-nasis et al is associated with the reorganization of apoA-Ⅰ gene and aPOC-Ⅲ gene.