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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.