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采用缺氧诱导体外培养血管内皮细胞凋亡模型, 用脂质体介导的基因转移法将含血管内皮生长因子(VEGF)cDNA的真核表达载体pSVI21 导入血管平滑肌细胞(VSMC) 中, 取此VSMC条件培养液, 再行血管内皮细胞(VEC) 培养, 用透射电镜、原位末端标记和流式细胞仪分析法观察VEGF对凋亡产生的影响。结果发现: 缺氧组凋亡发生率明显增加, 而加用转基因VSMC条件培养液后凋亡发生率明显减少, 并可减轻缺氧致内皮细胞超微结构的改变。结果表明: VEGF可减少缺氧诱导血管内皮细胞凋亡的产生, 保持血管内皮细胞的完整, 有益于防止或减少缺氧时内皮受损及内皮功能紊乱
The model of vascular endothelial cell apoptosis induced by hypoxia was established. The eukaryotic expression vector pSVI21 containing vascular endothelial growth factor (VEGF) cDNA was introduced into vascular smooth muscle cells (VSMCs) by liposome-mediated gene transfer method. VSMC conditioned medium was cultured in VEC. The effects of VEGF on apoptosis were observed by transmission electron microscopy, in situ terminal labeling and flow cytometry. The results showed that: the incidence of apoptosis in hypoxia group increased significantly, while the addition of transgenic VSMC conditioned medium significantly reduced the incidence of apoptosis, and can reduce the hypoxia induced endothelial cell ultrastructure changes. The results showed that: VEGF can reduce the hypoxia-induced apoptosis of vascular endothelial cells, maintain the integrity of vascular endothelial cells, beneficial to prevent or reduce endothelial dysfunction and endothelial dysfunction in hypoxia