慢性尼古丁对实验性血管壁斑块内皮细胞和平滑肌细胞增殖速率的影响。

T Strohschneider, M Oberhoff, H Hanke, A Hannekum, K R Karsch
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引用次数: 17

摘要

为了研究尼古丁、胆固醇摄食及其联合摄食对血管壁斑块内皮细胞和平滑肌细胞的影响,建立了一种实验方法,对这些刺激作用下内皮细胞和平滑肌细胞DNA合成的组分进行免疫组化检测和定量。为此,采用电刺激法在兔颈总动脉中产生标准化的纤维肌肉斑块。这些动物要么通过植入的渗透微型泵接受尼古丁,要么接受胆固醇饮食,或者两者兼而有之。在7天或14天后实验结束时测定斑块大小,以及暴露于溴脱氧尿苷(BrdU)期间内皮细胞和平滑肌细胞在DNA合成中的比例。与对照组相比,慢性尼古丁给药7天或14天内皮细胞BrdU标记指数明显升高。尼古丁和胆固醇饮食的结合导致了更显著的增加。相比之下,尼古丁给药后平滑肌细胞的BrdU标记指数没有增加。然而,与胆固醇喂养相比,尼古丁和胆固醇的结合导致斑块中平滑肌细胞的BrdU标记指数显著增加。对斑块大小的测量显示,在尼古丁摄入14天后,对照组和尼古丁治疗组的动物之间没有差异,而与单独接受胆固醇饮食的一组动物相比,胆固醇和尼古丁的组合产生了更多的斑块形成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of chronic nicotine delivery on the proliferation rate of endothelial and smooth muscle cells in experimentally induced vascular wall plaques.

To study the effect of nicotine, cholesterol feeding, and their combination on endothelial and smooth muscle cells in vascular wall plaques an experimental method was established which allows the immunohistochemical detection and quantification of the fractions of endothelial and smooth muscle cells in DNA synthesis under the effect of these stimuli. For this purpose standardized fibromuscular plaques were produced by electrostimulation in the common carotid arteries of rabbits. The animals received either nicotine via implanted osmotic minipumps or a cholesterol diet or both. Plaque size was determined at the end of the experiments after 7 or 14 days as well as the fraction of endothelial and smooth muscle cells in DNA synthesis during exposure to bromodeoxyuridine (BrdU). The BrdU labeling index of endothelial cells clearly increased under chronic nicotine administration for either 7 days or 14 days compared to controls. The combination of nicotine and cholesterol diet led to a more significant increase. In contrast, the BrdU labeling index of smooth muscle cells was not increased under nicotine delivery. The combination of nicotine and cholesterol, however, led to a significant increase of the BrdU labeling index of smooth muscle cells in the plaques compared to cholesterol feeding. Measurement of the plaque size revealed no difference between controls and nicotine-treated animals after 14 days of nicotine delivery, whereas the combination of cholesterol and nicotine produced increased plaque formation compared to a group of animals which received a cholesterol diet alone.

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