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兔胆固醇诱导动脉粥样硬化早期阶段的胶原蛋白代谢

Collagen metabolism during the early stages of cholesterol-induced atherogenesis in rabbits.

作者信息

Langner R O, Modrak J B

出版信息

Blood Vessels. 1976;13(5):257-66. doi: 10.1159/000158096.

DOI:10.1159/000158096
PMID:974270
Abstract

The involvement of collagen in cholesterol-induced atherosclerosis in rabbits was investigated. Rabbits were fed a 2% cholesterol diet for 8, 16, 30, 60 and 90 days. Histological sections were taken and aortic free and esterified cholesterol were determined after separation on thin-layer chromatography. Prolyl hydroxylase activity was used as a measure of collagen synthetic rate and hydroxyproline levels as an estimate of collagen content. Cholesterol content was a significantly increased after 8 days, while at this time there were no gross aortic lesions. After 30 days there was some aortic disease and by 60 days most of the rabbits exhibited pronounced aortic lesions. Histologically, the lesions consisted mainly of intimal foam cells. There was no alteration in collagen synthetic rate or content at 8, 16, 30 or 60 days. These data indicate that 60 days of continuous cholesterol feeding results in a foam cell aortic lesion with no alteration in collagen metabolism. After 90 days of cholesterol feeding there was significant increase in collagen synthetic activity in the thoracic aorta. These data suggest that alteration of collagen synthetic activity is secondary response, resulting from injury induced by the aortic accumulation of large amounts of cholesterol.

摘要

研究了胶原蛋白在兔胆固醇诱导的动脉粥样硬化中的作用。给兔子喂食含2%胆固醇的饮食,持续8、16、30、60和90天。取组织学切片,并在薄层色谱分离后测定主动脉游离胆固醇和酯化胆固醇。脯氨酰羟化酶活性用作胶原蛋白合成速率的指标,羟脯氨酸水平用作胶原蛋白含量的估计值。8天后胆固醇含量显著增加,而此时主动脉没有明显病变。30天后出现一些主动脉疾病,到60天时,大多数兔子出现明显的主动脉病变。组织学上,病变主要由内膜泡沫细胞组成。在8、16、30或60天时,胶原蛋白合成速率或含量没有变化。这些数据表明,连续60天喂食胆固醇会导致泡沫细胞主动脉病变,而胶原蛋白代谢没有改变。喂食胆固醇90天后,胸主动脉中胶原蛋白合成活性显著增加。这些数据表明,胶原蛋白合成活性的改变是一种继发反应,是由大量胆固醇在主动脉中蓄积引起的损伤所致。

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Collagen metabolism during the early stages of cholesterol-induced atherogenesis in rabbits.兔胆固醇诱导动脉粥样硬化早期阶段的胶原蛋白代谢
Blood Vessels. 1976;13(5):257-66. doi: 10.1159/000158096.
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