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应用人血清清蛋白代替LDS,建立了肝素释放细胞表面与受体结合的LDL的方法,并比较了人及家兔LDL结合家兔细胞表面受体的能力。在37℃不同保温时间(从0—180分钟),肝素释放的细胞表面受体~(125)I-LDL量增加缓慢而通过受体进入细胞的LDL量增加迅速。在37℃以不同剂量的LDL(13—78μg/ml)与细胞保温2小时,肝素释放的细胞表面受体LDL量也增加缓慢,而进入细胞的量增加更为迅速。结果显示LDL在细胞表面受体部位不断进入细胞内并迅速被新的LDL分子所取代,但当LDL增至78μg/ml时逐渐变慢,与Goldstein观察相似。肝素释放的~(125)LDL量在加入量约50 μg/ml时呈现平坦,与Goldstein观察相似。这说明用人血清清蛋白代替LDS同样可以观察到LDL受体的饱和特性。在同一实验条件下。肝素释放家兔的~(125)I-LDL比人高l倍,家兔通过受体进入细胞的~(125)I-LDL比人高1.7倍。二者差别非常显著(P<0.001)。显示兔血清LDL的结构可能在某些方面不同于人。
Human serum albumin was used instead of LDS to establish a method for heparin to release LDL on the cell surface and its receptor. The ability of human and rabbit LDL to bind to the receptor on the surface of rabbit cells was also compared. At 37 ° C for different incubation times (from 0 to 180 minutes), the amount of ~ (125) I-LDL on heparin-released cell surface receptors increased slowly and the amount of LDL entering the cells through the receptor increased rapidly. The amount of LDL released from heparin-released cell surface receptors also increased slowly with a different dose of LDL (13-78 μg / ml) at 37 ° C for 2 hours, and the amount entering the cells increased more rapidly. The results showed that LDL continued to enter cells at the cell surface receptor sites and was rapidly replaced by new LDL molecules, but gradually slowed down as LDL increased to 78 μg / ml, similar to Goldstein’s observation. The amount of ~ (125) LDL released by heparin was flattened at about 50 μg / ml, similar to Goldstein’s observations. This shows that the use of human serum albumin instead of LDS can also be observed LDL receptor saturation characteristics. Under the same experimental conditions. The ~ (125) I-LDL in heparin-released rabbits is 1-fold higher than in humans and the ~ 125 I-LDL in rabbits that enters the cells through the receptor is 1.7-fold higher than in humans. The difference between the two was significant (P <0.001). The structure of rabbit serum LDL is shown to be different in some ways from human.