氧化型低密度脂蛋白对人巨噬细胞超微结构的影响

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目的探讨氧化型低密度脂蛋白(OX-LDL)对人巨噬细胞超微结构的影响。方法体外培养人单核细胞系THP-1细胞,经100 nmol.L-1佛波酯(PMA)作用24 h,使其分化成人巨噬细胞,经终质量浓度为50 mg.L-1的OX-LDL分别诱导4 h及24 h,收集细胞,并制作细胞电镜标本。采用JEM1230型透射电镜观察。同时将未加入OX-LDL诱导的人巨噬细胞作为对照组。结果经OX-LDL诱导后的人巨噬细胞超微结构随时间发生动态变化,细胞内脂滴明显增多,内质网扩张、部分或完全脱颗粒,核膜发泡、不完整,染色质浓缩、碎裂,并形成典型的凋亡小体。另外,在OX-LDL诱导24 h的处理组细胞内发现自噬小体。而对照组未经OX-LDL诱导后的人巨噬细胞超微结构随时间无明显改变,细胞内仅见少量脂滴,内质网无扩张,未出现脱颗粒现象,核膜完整,染色质无碎裂,未形成凋亡小体。另外,在未经OX-LDL诱导24 h的对照组细胞内无自噬小体形成。结论OX-LDL在诱导人巨噬细胞形成泡沫细胞的同时发生细胞凋亡及自噬现象。 Objective To investigate the effect of oxidized low density lipoprotein (OX-LDL) on the ultrastructure of human macrophages. Methods Human monocytic THP-1 cells were cultured in vitro and were differentiated into human macrophages by 100 nmol.L-1 phorbol ester (PMA) for 24 h. After the final concentration of 50 mg.L-1 OX-LDL were induced 4 h and 24 h, cells were collected, and the preparation of cell electron microscopy specimens. Using JEM1230 transmission electron microscope observation. At the same time, OX-LDL-induced human macrophages were not included as control group. Results The ultrastructure of human macrophages induced by OX-LDL changed dynamically with time, the number of intracellular lipid droplets increased significantly, the endoplasmic reticulum was dilated, partially or completely degranulated, the nuclear membrane foamed, incomplete, chromatin condensation , Fragmentation, and the formation of typical apoptotic bodies. In addition, autophagosomes were found in cells treated with OX-LDL for 24 h. In the control group, the ultrastructure of human macrophages did not change significantly with the passage of time after OX-LDL induction. There were only a few lipid droplets in the cells, no expansion of the endoplasmic reticulum, no degranulation, complete nuclear membrane, and no chromatin Fragmentation, did not form apoptotic bodies. In addition, autophagosome formation was not observed in control cells exposed to OX-LDL for 24 h. Conclusion OX-LDL induces apoptosis and autophagy simultaneously with the formation of foam cells in human macrophages.
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