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机构地区:[1]南京医科大学病理生理研究室
出 处:《生物化学杂志》1996年第3期332-335,共4页
摘 要:应用经PMA诱导衍生的THP-1巨噬细胞为模型,以单克隆抗体C7B封闭oxLDL上的LDL受体结合位点,结果发现,正常细胞在摄取oxLDL时LDL受体与清道夫受体起协同作用;但C7B作用于蓄积了脂质的THP-1巨噬细胞时,对细胞脂质蓄积程度无明显影响,清道夫受体活性不但不降低反而有所升高,说明由于脂质蓄积LDL受体的作用减弱.Macrophages induced from THP-1 cells by PMA were used as the cell model. Mab C7B,the monoclonal antibody directed against LDL receptor binding domain on apolipoprotein B molecules was incubated with oxidized LDL at 4℃ overnight to inhibit the intake by THP-1 macrophages from LDL receptor pathway.It was found that 50μg/ml Mab C7B could reduce significantly the binding and degradation of (125) ̄I-oxLDL by cells. When THP-1 macrophages were loaded with oxLDL+C7B for 72 h,the amount of cholesteryl ester was not significantly different from that in control cells loaded with oxLDL only. The activity of scavenger receptor was enhanced significantly as compared with the control.These results indicated that LDL receptor reacted synergicly with scavenger receptor in the intake of oxLDL by normal macrophages,but it had no effects on the accumulation of cholesteryl ester in the cells.
分 类 号:R543.502[医药卫生—心血管疾病]
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