2,2’-盐酸脒基丙烷对ApoB100的氧化作用  

Oxidation of ApoB100 by AAPH

作　　者：王贞[1] 喻红[1] 洪嘉玲[1] 李小明[1] 

机构地区：[1]武汉大学医学院生物化学与分子生物学系,武汉430071

出　　处：《武汉大学学报（医学版）》2004年第3期236-238,248,共4页Medical Journal of Wuhan University

摘　　要：目的 :探讨载脂蛋白B1 0 0 (ApoB1 0 0 )的体外氧化状态与其基本性质变化之间的关系。方法 :采用多聚阴离子沉淀、短时密度梯度超速离心法得到纯化的低密度脂蛋白 (LDL) ,经有机试剂抽提脂质 ,由半制备型分子排阻型高效液相色谱进一步纯化得到ApoB1 0 0。 2 ,2’ 盐酸脒基丙烷 (AAPH)氧化ApoB1 0 0 ,经反相高效液相色谱分析其疏水性质。结果 :体外轻微氧化ApoB1 0 0不会导致其降解 ,但其疏水性会增强。结论 :AAPH氧化ApoB1 0 0所致的早期疏水性改变 ,可能与LDL被清道夫受体识别有关 。Objective: To investigate the relationship between oxidation of ApoB100 and its hydrophobic changes. Methods: To isolate low density lipoprotein (LDL) by using polyanions precipitation and short time density gradient ultracentrifugation.Organic reagents were used to delipidate LDL and ApoB100 was further purified by semi preparative size exclusion high pressure liquid chromato graphy(HPLC). After incubat with AAPH,the oxidized ApoB100 was loaded on reverse phase HPLC to analyze its hydrophobic changes. Results: Mild oxidation in vitro did not lead to ApoB100 fragmentation, but could increase its hydrophobicity. Conclusion: Oxidation of ApoB100 by AAPH increases its hydrophobicity at early stage,suggesting that hydrophobic changes of ApoB100 induced by AAPH may relate to LDL recognition by scavenger receptor,which may be included in pathophysiology of atherosclerosis.

关 键 词：低密度脂蛋白 APOB100 氧化 自由基 疏水性 

分 类 号：R541.4[医药卫生—心血管疾病]