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目的探讨氧化修饰低密度脂蛋白（ｏｘｉｄａｔｉｖｅｌｙｍｏｄｉｆｉｅｄｌｏｗｄｅｎｓｉｔｙｌｉｐｏｐｒｏｔｅｉｎ，ｏｘＬＤＬ）导致动脉粥样硬化形成的途径及可能机制。方法在体外培养的小牛主动脉内皮细胞（ｂｏｖｉｎｅａｏｒｔｉｃｅｎｄｏｔｈｅｌｉａｌｃｅｌ，ＢＡＥＣ）中加入ｏｘＬＤＬ，终浓度为０．１ｍｇＰｒ／ｍｌ，培养２４ｈ后，采用细胞毒试验、流式细胞仪、丙二醛（ＭＤＡ）测定及细胞计数等方法分别对其贴壁细胞及培养液进行了检测。结果加ｏｘＬＤＬ组与对照组（未加ｏｘＬＤＬ组）相比，发现：①在相差显微镜下，ｏｘＬＤＬ组细胞形态明显拉长，发生脱落，并存在大片脱失区；②细胞毒试验发现ｏｘＬＤＬ对ＢＡＥＣ的生长增殖有明显的抑制作用；③流式细胞仪检测发现ｏｘＬＤＬ抑制ＢＡＥＣ由Ｇ１期进入ＤＮＡ合成的Ｓ期，且ｏｘＬＤＬ可诱导ＢＡＥＣ凋亡的发生；④ＭＤＡ检测发现ｏｘＬＤＬ促进ＢＡＥＣ脂质过氧化物生成；⑤加ｏｘＬＤＬ组ＢＡＥＣ粘附的ＨＬ６０细胞数明显多于对照组。结论由ｏｘＬＤＬ作用引起的内皮细胞形态损伤、增殖抑制、脂质过氧化物生成增多及单核细胞粘附性增加等改变可能是动脉粥样硬化形成的机制之一。
Objective To investigate the pathways and possible mechanisms of atherosclerosis induced by oxidatively modified low density lipoprotein (oxLDL). Methods oxLDL was added into bovineorticendothelialcel (BAEC) cultured in vitro at a final concentration of 0.1 mgPr / ml. After incubation for 24 h, cytotoxicity assay, flow cytometry, malondialdehyde (MDA) assay And cell counting methods such as adherent cells and culture were tested. Results Compared with the control group (without oxLDL group), oxLDL group showed that: (1) under the phase contrast microscope, the cell morphology of oxLDL group was significantly elongated, shedding occurred and there was a large area of missing area; (2) cytotoxicity assay showed that oxLDL inhibited BAEC ③ Flow cytometry showed that oxLDL could inhibit the BAEC from G1 phase into the S phase of DNA synthesis, and oxLDL could induce the apoptosis of BAEC. ④MDA assay found that oxLDL promoted BAEC lipid peroxides The number of HL60 cells adherent to BAEC in oxLDL group was significantly more than that in control group. Conclusion The changes of endothelial cell morphology, inhibition of proliferation, increased production of lipid peroxides and monocyte adhesion caused by oxLDL may be one of the mechanisms of atherosclerosis.