修饰的脂蛋白(a)在动脉粥样硬化中的作用

本文观察了体外丙二醛（MDA）修饰的脂蛋白（a）Lp（a）]结构与生物学性质的变化。硫代巴比妥酶活性物质实验（TBARS）和脂蛋白琼脂糖电泳显示经MDA修饰后，Lp（a）脂质过氧化程度增高，负电荷增多．小鼠腹腔巨噬细胞脂质蓄积实验和对125I－MDA－LDL降解抑制实验揭示，丙二醛修饰的Lp（a）较天然Lp（a）更明显提高鼠腹腔巨噬细胞对胆固醇酯的蓄积和对125I－MDA－LDL降解的抑制，证实了Lp（a）经丙二醛修饰后易被巨噬细胞-清道夫受体识别和摄取，导致细胞内胆固醇酯的蓄积和泡沫细胞的形成，参与动脉粥样硬化的病理过程。此外，通过比较MDA－Lp（a）与MDA-LDL氧化修饰的难易度和对巨噬细胞脂质蓄积的影响，提示Lp（a）分子中载脂蛋白apoB－100在丙二醛修饰Lp（a）中起主要作用。

Effects of modified lipoprotein(a) on the atherosclerosis

The changes in the structure and biological properties of malondialdehyde modified Lp (a) in vitro were observed. The assays of thiobarbituric acid-reactive substances and lipoprotein agarose gel electrophoresis indicated that after being modified by malondialdehyde, Lp (a) showed enhanced lipid peroxidation and increased negative change. Relative to native Lp (a),modified Lp (a) markedly elevated the accumulation of cholesterol ester in mouse peritoneal macrophages and reduced the degradation of 125I-modified LDL by mouse peritoneal macrophage. Experimental evidences indicated that rnodified Lp (a) can easily be recognized and uptaken by macrophages-scavenger receptor,resulting in the accumulation of cholesterol ester and formation of macrophage-derived foam cells and involving in the pathologic procedure of athprosclerosis. In addition, by comparing the degress of oxidative modification and the influence on the accumulation of cholesterol ester in macrophages,it is implied that apoB100 in Lp (a) may play a main role in the procedure of modifying Lp (a) by malondialdehyde.