论文部分内容阅读
目的：探讨氧化型低密度脂蛋白（ＯＸ－ＬＤＬ）对血管内皮细胞调亡的影响及其可能的调控机制。方法：以 ０．１μｇ／Ｌ和０．３μｇ／Ｌ的 ＯＸ－ＬＤＬ作用培养的人脐静脉血管内皮细胞（ＥＣ）４ｈ，采用流式细胞仪碘化丙啶染色法检测细胞凋亡；提取细胞ＤＮＡ，采用琼脂糖凝胶电泳，观察凋亡细胞ＤＮＡ梯形带；提取细胞ＲＮＡ，采用逆转录一聚合酶链式反应（ＲＴ－ＰＣＲ）技术检测Ｆａｓ抗原基因表达。结果：ＯＸ－ＬＤＬ处理能诱导ＥＣ凋亡，并存在一定的剂量效应关系，ＤＮＡ电泳亦显示高剂量ＯＸ－ＬＤＬ处理能产生的ＤＮＡ片断比低剂量时更明显，而对照组无明显ＤＮＡ梯形带出现。基础状态下ＦＥＣ表达Ｆａｓ抗原基因甚微，ＯＸ－ＬＤＬ处理诱导其表达，并存在剂量依赖关系。结论：ＯＸ－ＬＤＬ诱导ＥＣ凋亡，Ｆａｓ抗原基因表达上调可能是调控机制之一。
Objective: To investigate the effect of oxidized low density lipoprotein (OX-LDL) on the apoptosis of vascular endothelial cells and its possible regulatory mechanism. Methods: Cultured human umbilical vein endothelial cells (ECs) were incubated with OX-LDL at 0.1μg / L and 0.3μg / L for 4 hours. The apoptosis of cells was detected by flow cytometry with propidium iodide staining. DNA was extracted by agarose gel electrophoresis and DNA ladder of apoptotic cells was observed. RNA was extracted and the gene expression of Fas antigen was detected by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: OX-LDL treatment induced EC apoptosis with dose-response relationship. DNA electrophoresis also showed that DNA fragments produced by high-dose OX-LDL treatment were more obvious than those treated with low dose of DNA, while DNA ladder was not found in the control group appear. Under the basal state FEC expression of Fas antigen gene is very small, OX-LDL treatment induced its expression, and there is a dose-dependent relationship. Conclusion: OX-LDL induces apoptosis of EC and up-regulation of Fas antigen gene expression may be one of the regulatory mechanisms.