氧化极低密度脂蛋白促进猪主动脉平滑肌细胞内脂类堆积的机制及其细胞毒作用

Mechanism of Lipid Accumulation in Swine ASMC Caused by OX-VLDL and the SMC-toxic Effect of OX-VLDL

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。

Oxidatively modified very low density lipoprotein(OX-VLDL).(200 μg-TG/ml ) wereincubated with swine aortic smooth muscle cells(SMC) for 48 hours, causing a 3. 2 fold increment of cellular TG (P<0. 01) and a 1. 22 fold increment of cellular TC (P<0. 05) in SMC. FITC-OX-VLDL were taken up bySMC via saturable mechanism. Scatchard plot of the data showed that Kd was 48. 82 μg/ml and Bmax was2 067 ng OX-VLDL/mg cell protein. N-LDL competed with FITC-OX-VLDL on binding to SMC asefficiently as OX-VLDL. It was also found that some cells were damaged when smooth muscle cells were incubatedwith OX-VLDL for more than 24 hours. The results suggest that OX-VLDL may contribute to lipidaccumulation in SMC and be of importance in the conversion of SMC to foam cells. The SMC-toxic effect ofOXVLDL may contribute to the rupture of atherosclerotic plaque.