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目的：探讨氧化低密度脂蛋白（ｏｘｉｄｉｚｅｄ ｌｏｗ ｄｅｎｓｉｔｙｌｉｐｏｐｒｏｔｅｉｎ，ｏｘＬＤＬ） 血管内皮受体（ｌｅｃｔｉｎｌｉｋｅ ｏｘＬＤＬｒｅｃｅｐｔｏｒ，ＬＯＸ１）在ｏｘＬＤＬ致内皮细胞损伤中的作用及其机制。方法：放射配基结合及竞争抑制实验检测人脐静脉内皮细胞（ｈｕｍａｎ ｕｍｂｉｌｉｃａｌｖｅｉｎ ｅｎｄｏｔｈｅｌｉａｃｅｌｌｓ，ＨＵＶＥＣｓ）存在ＬＯＸ１ 的高亲和位点，采用倒置相差显微镜观察细胞形态的改变，测定细胞及上清乳酸脱氢酶（ｌａｃｔｉｃ ｄｅｈｙｄｒｏｇｅｎａｓｅ，ＬＤＨ）活性，计算细胞死亡率，发色底物法检测内皮细胞培养液中的组织纤溶酶原激活物（ｔｉｓｓｕｅ ｐｌａｓｍｉｎｏｇｅｎ ａｃｔｉｖａｔｏｒ，ｔＰＡ） 和纤溶酶原激活物抑制剂（ｐｌａｓｍｉｎｏｇｅｎａｃｔｉｖａｔｏｒｉｎｈｉｂｉｔｏｒ１ ，ＰＡＩ１）的活性； 反转录聚合酶链反应检测ＬＯＸ１ ｍＲＮＡ 表达水平，Ｃａ２＋ 示踪测定细胞钙转运功能。结果：ＨＵＶＥＣｓ 存在ＬＯＸ１ 的高亲和位点［Ｂｍａｘ（５４ ±２０） ｎｇ／１０６ ｃｅｌｌｓ，Ｋｄ（２．０ ±０．６） ×１０－８ ｍｏｌ·Ｌ－ １］ ，单纯加入ｏｘＬＤＬ作用２４ ｈ ?
AIM: To investigate the role and mechanism of oxidized low density lipoprotein (oxLDL) -induced endothelial progenitor cells (LOX1) in endothelial cell injury induced by oxLDL. Methods: Radioligand binding and competition inhibition assay were used to detect the high affinity sites of LOX1 in human umbilicalvein endothelia cells (HUVECs). The morphological changes of cells were observed by inverted phase contrast microscope. The activity of lactic dehydrogenase (LDH) was calculated to calculate the cell death rate. The chromogenic substrate method was used to detect the inhibitory effect of tissue plasminogen activator (tPA) and plasminogen activator (Plasminogen activator inhibitor 1, PAI 1) activity; reverse transcription polymerase chain reaction LOX1 mRNA expression levels detected by Ca2 + tracer cells calcium transport function. Results: There was a high affinity site of LOX1 in HUVECs [Bmax (54 ± 20) ng / 106 cells, Kd (2.0 ± 0.6) × 10-8 mol·L-1] 24 h?