神经节苷脂类抑制BT325细胞系生长机理的初步探讨  

Preliminary Studies on Machanism of Inhibition of Gangliosides on BT325 Line Growth.

作　　者：李爱华[1] 杨典洱[1] 陈红[1] 黄如彬[1] 

机构地区：[1]首都医科大学生物化学教研室

出　　处：《生物化学与生物物理进展》1999年第3期250-254,共5页Progress In Biochemistry and Biophysics

摘　　要：用１２５ＩＥＧＦ与人多形成胶质细胞瘤ＢＴ３２５细胞系膜上ＥＧＦ受体的饱和结合实验，竞争抑制实验研究ＧＭ３，ＢＢＧ（ｂｏｖｉｎｅｂｒａｉｎｇａｎｇｌｉｏｓｉｄｅｓ）对ＥＧＦ受体最大结合量，亲和常数及受体数目的影响；放射受体法观察ＥＧＦＥＧＦＲ复合物内吞过程，测定胞质和培养基中ＥＧＦ含量．结果表明：ＢＴ３２５细胞质膜上存在高亲和力ＥＧＦ结合位点，ＧＭ３对ＥＧＦ与其受体的亲和力无明显抑制作用（Ｐ＞００５），但能明显减少其受体的数目（Ｐ＜００５）；ＧＭ３能明显延长ＥＧＦＥＧＦＲ复合物内吞过程；ＧＭ３处理的胞质中ＥＧＦ浓度比对照组显著升高（Ｐ＜００５），培养液中无明显差异。Radioligand binding assay and competitive radio assay of 125 I EGF on plasma membrance EGF receptor and radio receptor assay when 125 I EGF was incubated with human glioblastoma multiforme cells were carried out. The results showed that there is a high affinity binding site on BT325 cells plasma membrance, exogenous GM3 could not alter the affinity ( K d) of EGF binding with cell surface receptors, but decrease the receptor number. GM3 could significantly prolong the endocytosis process of EGF EGFR complex. The concentration of EGF in culture medium was unchanged by GM3 and BBG,but that of EGF in cytoplasm was increased by GM3. It suggested that GM3 might inhibit the secretion of EGF.

关 键 词：BT325细胞系 神经节苷脂GM3 抑瘤作用 

分 类 号：Q546[生物学—生物化学] Q26