摘要
Using splenic cells of BALB/c mice infected with Friend Leukemia Virus (FVA) as a model of erythroid cells, we investigated the action of dexamethasone (Dex) to induce apoptosis of the cells in the presence of erythropoietin (EPO)——an apoptotic inhibitor in developing erythroid cells. The result indicated that after treatment with a certain range of Dex concentrations and prolonged incubation, the cells were characterized by the occurrence of DNA ladders which appeared on agarose electrophoresis. Transmission electron microscopy showed that karyopyknosis, chromatin condensation, dilatation of the perinuclear space, karyorrhexis, cytoplasmic vacuolization and cell fragmentation appeared in the cells depending on the dose of Dex and the treatment time. These results suggest that Dex could induce apoptosis in the developing erythroid cells as in other cells so far reported.
正常机体内，红细胞生成素（ＥＰＯ）诱导红系细胞分化，并阻止其凋亡，使其维持机体所需足够的数量。本文采用诱发贫血病毒（ＦＶＡ）诱导ＢＡＬＢ／ｃ小鼠脾细胞所形成的红细胞为实验系统，研究了外界因子？？地塞米松（Ｄｅｘ）对ＥＰＯ作用的影响。取６８周雌性ＢＡＬＢ／ｃ小鼠，尾部静脉注射含ＦＶＡ的小鼠血清。１５天后，断颈处死。取脾于ＩＭＤＭ中漂洗、剪碎、过滤、离心、制成单细胞悬液，在ＥＰＯ存在下，于平皿中培养至不同的时期后，进行不同浓度、不同时间的Ｄｅｘ处理。取细胞进行：（１）台盼蓝染色计数死细胞数；（２）观察ＤＮＡ电泳图谱；（３）电镜检察细胞学变化。Ｆｉｇ．１表明：随着Ｄｅｘ处理浓度和时间的增加，细胞死亡率也增加。Ｆｉｇ．２表明：１０－４浓度Ｄｅｘ处理，即可使早（１２ｈ）、中（２４ｈ）幼期红细胞凋亡，ＤＮＡ断裂成多聚核小体，产生明显ＤＮＡ梯形带。Ｆｉｇ．３表明：高浓度Ｄｅｘ可以使早幼期红细胞凋亡。电镜观察表明：与对照（Ｆｉｇ．４）比较，Ｄｅｘ处理后，细胞核固缩，染色质沿核膜内面周边凝聚，核周间隙扩张，胞质内出现空泡（Ｆｉｇ．５）；随后细胞破碎，出现大量凋亡小体（Ｆｉｇ．６）。Ｄｅｘ拮抗ＥＰＯ，诱导红系细胞凋亡的现象此?
