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目的研究全反式维甲酸在视网膜母细胞瘤裸鼠移植瘤成瘤过程中的诱导分化作用及可能的机理。方法用腋部皮下注射SO-RB50细胞的方法对裸小鼠造模,定期观察肿瘤体积及重量、病理、电镜超微结构,增殖活性,检测各组肿瘤中CycinD1、CDK4、ICAM的表达水平。结果试验结束时给药组平均瘤重(2.750±0.302)g,于对照组的(7.150±1.228)g(P=0.008)及维甲酸缺乏组的(11.483±2.721)g(P=0.003)。镜检给药组肿瘤细胞大片出血坏死,对照组与原移植瘤的病理表现相同,维甲酸缺乏组核浆比大,核染色较对照组深。电镜示给药组细胞线粒体明显肿胀,空泡化,核糖体较对照组明显减少。对照组细胞同原移植瘤一致。维甲酸缺乏组游离核糖体较对照组多,溶酶体少见。给药组与对照组CyclinD1(P=0.012)、CDK4(P=0.010)差异有统计学意义,ICAM-1(P=0.071)未见有显著统计学差异;维甲酸缺乏组与对照组,CyclinD1(P=0.017)、CDK4(P=0.029)差异有统计学意义,ICAM-1(P=0.083)未见有显著统计学差异。结论维甲酸抑制视网膜母细胞瘤生长,维甲酸缺乏可促进视网膜母细胞瘤的生长,诱导分化作用的实现与调节CyclinD1和CDK4的表达水平有关。
Objective To study the induction and differentiation of all-trans retinoic acid in tumorigenesis of retinoblastoma xenografts in nude mice and its possible mechanism. Methods The nude mice were injected subcutaneously with SO-RB50 cells in the axilla and the tumor volume, weight, pathology, ultrastructure and proliferative activity of the tumor were observed regularly. The expression of CycinD1, CDK4 and ICAM in each group were detected. Results The mean tumor mass (2.750 ± 0.302) g at the end of the experiment was 7.150 ± 1.228 g (P = 0.008) in the control group and (11.483 ± 2.721) g in the retinoic acid-deficient group (P = 0.003). Microscopic examination of the tumor cells hemorrhage and necrosis in the control group, the control group and the original pathological manifestations of xenografts, retinoic acid deficiency nucleoplasmic large nuclear staining compared with the control group. Electron microscopy showed that the mitochondria of the treated group were obviously swollen and vacuolated, and the ribosomes were significantly reduced compared with the control group. The control group of cells with the original transplanted tumor consistent. Retinoid deficiency group free ribosome more than the control group, lysosome rare. The difference between CyclinD1 (P = 0.012) and CDK4 (P = 0.010) in treatment group and control group was statistically significant. There was no significant difference between ICAM-1 and control group (P = 0.071) (P = 0.017) and CDK4 (P = 0.029). There was no significant difference in ICAM-1 (P = 0.083). Conclusion Retinoic acid inhibits the growth of retinoblastoma. Retinoic acid deficiency can promote the growth of retinoblastoma. The induction of differentiation is related to the regulation of the expression of CyclinD1 and CDK4.