【摘要】 目的 :研究氧化低密度脂蛋白ox LDL对血管内皮细胞VEC粘附分子 (ICAM 1,VCAM 1)和单核细胞趋化蛋白 1(MCP 1)表达 ,以及单核细胞(MC)跨膜迁移的影响 ,以阐明ox LDL促AS形成的作用。方法 :以含 2 0 0mg·L- 1ox LDL的M199培养液处理脐静脉内皮细胞 (HUVEC) ,收集细胞和培养上清液 ,以免疫组化卵白素生物素复合法 (ABC法 )、ELISA法测量细胞上ICAM 1和VCAM 1表达 ,以夹心ELISA法测定培养上清液中MCP 1蛋白浓度 ,采用逆转录 -聚合酶链反应RT PCR方法测定VEC中ICAM 1和MCP 1mRNA的表达 ,以微趋化小室测定ox LDL对MC的趋化作用。结果 :HUVEC暴露于ox LDL中 2 4h后 ,VEC上ICAM 1及其mRNA表达显著增加。MCP 1mRNA及MCP 1蛋白表达显著增加 ,同时可见细胞收缩变圆 ,细胞间隙加大 ,显示ox LDL对VEC有较强的细胞毒性 ,ox LDL可引起MC跨膜迁移增加。结论 :ox LDL可引起VEC介导MC粘附和趋化的物质表达显著增加及损伤 ,有利于MC和脂质向内皮下侵入 ,这些结果表明ox LDL在AS形成中起重要作用。更多还原

【Abstract】 AIM: To study the effects of oxidized low density lipoprotein (ox LDL) on the formation of atherosclerosis. METHODS: Human umbilical vein endothelial cell (HUVEC) was exposured to ox LDL (200 mg·L -1 ) for 24 h, the cell and culture supernat was measured by Sandwich ELISA, the total RNA was extracted from HUVEC by the guanidinium isothiocyanate, ICAM 1 mRNA and MCP 1 mRNA expression in HUVEC were measured by RT PCR (reverse transcription polymerase chain reaction). ICAM 1 and VCAM 1 expression on HUVEC were determined by using immunohistochemistry ABC. RESULTS: After exposure to ox LDL 24 h, ICAM 1 and its mRNA, MCP 1 mRNA and protein expression were markedly increased in HUVEC, and ox LDL caused cells to retract and increase gaps between cells, and to increase human monocyte transmembrane migration. CONCLUSION: ox LDL accelerates monocyte and lipid to invade subendothelium and plays an important role in the formation of atherosclerosis.更多还原