Peng S K, Hu B, Hsiao W, Morin R
Department of Pathology, UCLA School of Medicine, Torrance 90509.
Artery. 1990;17(2):84-95.
Human umbilical vein endothelial cells and rabbit aortic smooth muscle cells in culture were incubated for intervals up to 24 hrs with varying concentrations of cholesterol, 7-ketocholesterol, 25-hydroxycholesterol, cholestane-3 beta,5 alpha,6 beta-triol or cholesterol-5 alpha, 6 beta-epoxide. Endocytosis, as measured by uptake of horseradish peroxidase (HRP), was inhibited in a dose and time dependent manner in both endothelial and smooth muscle cell cultures by cholestane-3 beta,5 alpha,6 beta-triol and 25-hydroxycholesterol. Inhibition by 7-ketocholesterol in endothelial cells occurred only at higher concentrations, and cholesterol and cholesterol epoxide showed no significant inhibitory effects. The viability of the cells exposed to the cholesterol oxides at the concentrations that inhibited the uptake of HRP was not changed. Cholesterol oxides induce functional endothelial injury, not morphologically apparent, which may be involved in atherogenesis.
将培养的人脐静脉内皮细胞和兔主动脉平滑肌细胞与不同浓度的胆固醇、7-酮胆固醇、25-羟胆固醇、胆甾烷-3β,5α,6β-三醇或胆固醇-5α,6β-环氧化物一起孵育长达24小时。通过辣根过氧化物酶（HRP）摄取来测量的内吞作用，在两种内皮细胞和平滑肌细胞培养物中，均被胆甾烷-3β,5α,6β-三醇和25-羟胆固醇以剂量和时间依赖性方式抑制。7-酮胆固醇仅在较高浓度下才会抑制内皮细胞的内吞作用，而胆固醇和胆固醇环氧化物则未显示出明显的抑制作用。在抑制HRP摄取的浓度下暴露于胆固醇氧化物的细胞活力没有改变。胆固醇氧化物会诱导功能性内皮损伤，这种损伤在形态上并不明显，可能与动脉粥样硬化的发生有关。
