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200μg／ml的氧化极低密度脂蛋白（OX－VLDL）与猪主动脉平滑肌细胞（SMC）温育48h后，细胞内甘油三酯（TG）含量为不加脂蛋白对照组的3．2倍（P＜0．01），细胞内总胆固醇（TC）含量为对照组的1．22倍（P＜0．05）。荧光素异硫氰酸酯（FITC）标记OX－VLDL的结合试验表明：SMC可摄取完整的OX－VLDL（Kd=48．82μg／ml，Bmax=2067ng／mgcellprotein）。竞争抑制试验表明，OX－VLDL及正常低密度脂蛋白（N－LDL）均对FITC－OX－VLDL的结合摄取表现出明显的竞争作用，两者的作用相似。以上结果表明，SMC能通过受体途径可饱和性地摄取完整的OX－VLDL，进而形成泡沫细胞。同时还发现OX－VLDL与SMC长时间温育（24h以上）会损伤细胞，造成部分细胞脱落。这对动脉粥样硬化及急性冠状动脉综合征发病机制研究及其预防和治疗都有重要的指导意义。
After incubation with 200 μg / ml OX-VLDL and porcine aortic smooth muscle cells (SMCs) for 48 h, the intracellular triglyceride (TG) content was 3.2-fold higher than that without lipoprotein control (P <0.01), and the intracellular total cholesterol (TC) content was 1.22 times that of the control group (P <0.05). Binding assays of fluorescein isothiocyanate (FITC) labeled OX-VLDL showed that SMC uptake intact OX-VLDL (Kd = 48.82 μg / ml, Bmax = 2067 ng / mgcellprotein). Competitive inhibition assays showed that both OX-VLDL and normal low-density lipoprotein (N-LDL) showed a significant competitive effect on the uptake of FITC-OX-VLDL, both of which had similar effects. The above results indicate that SMC can uptake intact OX-VLDL through the receptor pathway to form foam cells. Also found OX-VLDL and SMC prolonged incubation (24h above) will damage the cells, causing some cells off. This is of atherosclerosis and acute coronary syndrome pathogenesis research and prevention and treatment have important guiding significance.