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糖尿病对主动脉内皮细胞增殖的影响。

The effect of diabetes on the proliferation of aortic endothelial cells.

作者信息

Santilli S M, Fiegel V D, Aldridge D E, Knighton D R

机构信息

Department of Surgery, University of Minnesota, Minneapolis.

出版信息

Ann Vasc Surg. 1992 Nov;6(6):503-10. doi: 10.1007/BF02000821.

DOI:10.1007/BF02000821
PMID:1463663
Abstract

Diabetic vascular disease is more severe, diffuse, and accelerated when compared to nondiabetic vascular disease. Endothelial cell injury or alteration in endothelial cell function is hypothesized to be the initial cellular event in the pathophysiology of diabetic vascular disease. We examined the effect of insulin-treated and untreated alloxan diabetes on the proliferation of rabbit aortic endothelial cells in vitro by growing thoracic aortic endothelial cells from alloxan diabetic rabbits in serum obtained from alloxan diabetic rabbits. Diabetes adversely affected the proliferation of aortic endothelial cells; the most significant decrease in cell proliferation was noted in untreated diabetic cells. Crossover studies between endothelial cells and serum from different groups revealed that diabetes slows endothelial proliferation by not only a serum effect but also an intrinsic cellular effect. These observations suggest that diabetes adversely affects the proliferation of aortic endothelial cells by changing cell and serum functions.

摘要

与非糖尿病性血管疾病相比,糖尿病性血管疾病更为严重、广泛且进展加速。内皮细胞损伤或内皮细胞功能改变被认为是糖尿病性血管疾病病理生理学中的初始细胞事件。我们通过在从四氧嘧啶糖尿病兔获得的血清中培养四氧嘧啶糖尿病兔的胸主动脉内皮细胞,研究了胰岛素治疗和未治疗的四氧嘧啶糖尿病对兔主动脉内皮细胞体外增殖的影响。糖尿病对主动脉内皮细胞的增殖产生不利影响;在未治疗的糖尿病细胞中观察到细胞增殖最显著的下降。不同组内皮细胞与血清之间的交叉研究表明,糖尿病不仅通过血清效应,还通过内在细胞效应减缓内皮细胞增殖。这些观察结果表明,糖尿病通过改变细胞和血清功能对主动脉内皮细胞的增殖产生不利影响。

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The effect of diabetes on the proliferation of aortic endothelial cells.糖尿病对主动脉内皮细胞增殖的影响。
Ann Vasc Surg. 1992 Nov;6(6):503-10. doi: 10.1007/BF02000821.
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Rabbit aortic smooth muscle cell culture. A model for the pharmacological study of diabetes-induced alterations in cell proliferation.兔主动脉平滑肌细胞培养。一种用于糖尿病诱导的细胞增殖改变药理学研究的模型。
J Pharmacol Methods. 1991 Nov;26(3):211-22. doi: 10.1016/0160-5402(91)90045-7.

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