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为观察小鼠肝癌H22细胞及正常肝细胞LDLR对人LDL的结合,并对这两种细胞内移及降解人LDL的功能进行分析比较,用125I标记LDL,对上述细胞LDLR进行受体饱和分析和单点分析。结果表明:(1)H22细胞及正常肝细胞可通过其LDLR结合、内移、降解人LDL;(2)H22细胞及正常肝细胞LDLR对人LDL的亲和性和特异性相同,但H22细胞Bmax明显增多;(3)两种细胞对人LDL的非特异性结合差异不明显,内移及降解人LDL的能力亦相同。提示小鼠肝癌H22细胞LDLR数目增多,亲和性及特异性未变,对LDL的内移和降解功能亦未改变。
To observe the binding of LDLR of human hepatoma H22 cells and normal hepatocytes to human LDL, and to analyze and compare the functions of these two kinds of intracellular migration and degradation of human LDL, labeling LDL with 125I, and receptor saturation analysis of the above cells LDLR. And single point analysis. The results showed that: (1) H22 cells and normal hepatocytes could bind to, degrade and degrade human LDL through their LDLR; (2) H22 cells and normal liver cells had the same affinity and specificity for human LDL, but H22 cells Bmax increased significantly; (3) The non-specific binding of human LDL to the two cells showed no significant difference, and the ability to migrate and degrade human LDL was the same. It was suggested that the number of LDLR in mouse hepatoma H22 cells increased, the affinity and specificity remained unchanged, and the function of LDL migration and degradation did not change.