Bourne L C, Lamb D J, Collis C S, O'Brien M, Leake D S, Rice-Evans C
International Antioxidant Research Centre, UMDS-Guy's Hospital, London, UK.
FEBS Lett. 1997 Sep 15;414(3):576-80. doi: 10.1016/s0014-5793(97)01075-2.
In this study, the interaction of ruptured cardiac myocytes with low density lipoprotein (LDL) has been investigated and the consequent extent of uptake by macrophages. The results show that lysate released from ruptured myocytes is capable of inducing LDL oxidation and that the resulting modified form is recognised and degraded by macrophages. Peroxyl radical scavengers inhibit the LDL oxidation but not the macrophage uptake suggesting that LDL can be modified by mechanisms that are independent of oxidative processes by intracellular constituents of cardiac myocytes.
在本研究中，已对破裂心肌细胞与低密度脂蛋白（LDL）的相互作用以及随后巨噬细胞的摄取程度进行了研究。结果表明，破裂心肌细胞释放的裂解物能够诱导LDL氧化，并且产生的修饰形式可被巨噬细胞识别并降解。过氧自由基清除剂可抑制LDL氧化，但不抑制巨噬细胞摄取，这表明LDL可通过心肌细胞内成分的与氧化过程无关的机制进行修饰。
