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作 者:刘晓东[1] 游潮[1] 吴波[1] 蔡博文[1] 张敏[2] 李强[2]
机构地区:[1]四川大学华西医院神经外科,四川成都610041 [2]四川大学华西医院同位素室,四川成都610041
出 处:《中国临床神经外科杂志》2004年第5期360-362,共3页Chinese Journal of Clinical Neurosurgery
摘 要:目的探讨5-[125I]-2'-脱氧尿苷(125IUdR)对大鼠C6胶质瘤细胞中嗜银核仁组织原区蛋白(AgNOR蛋白)和增殖细胞核抗原(PCNA)表达的影响。方法体外培养C6胶质瘤细胞,建立C6胶质瘤Wistar大鼠模型,合成125IUdR和127IUdR后于肿瘤原位局部注射,5日后处死动物取标本分别行AgNOR染色和PCNA免疫组织化学染色,计算AgNOR颗粒数目、面积和PCNA标记指数。结果125IUdR治疗组C6胶质瘤细胞的AgNOR颗粒计数和面积、PCNA标记指数分别为(1.70±0.42)个/细胞,(4.32±1.38)μm2/细胞,(36.87±14.51)%;对照组分别为(2.50±0.37)个/细胞,(7.01±1.97)μm2/细胞,(52.24±10.86)%,两组相比均相差显著(P<0.05)。结论125IUdR可掺入肿瘤细胞DNA的合成中,选择性的杀伤S期的肿瘤细胞,显著的抑制C6胶质瘤细胞中AgNOR和PCNA的表达,从而抑制胶质瘤细胞的增殖。Objective To investigate the effect of 5- iodo-2′-deoxyuridine (125IUdR) on the expressions of argyrophilic nucleolar organizer regions (AgNOR) proteins and proliferating cell nuclear antigen (PCNA) of C6 glioma cells in Rats. Methods After culturing the C6 glioma cells, we established a model of C6 glioma in rats, 125IUdR and 127IUdR, which were synthesized, were separately injected into the tumor tissues respectively in the experimental and control groups. The expressions of AgNOR and PCNA in the fresh tumor tissues which were taken 5 days after the injection of the agents in both the groups, were determined respectively by argyrophilic stain and immunohistochemical technique. The number of argyrophilic grains, the solver-stained area and PCNA labeling index were measured. Results The number of argyrophilic and silver-stained area was 1.70±0.42/cell and (4.32±1.38)μm2/cell respectively in the experimental group, and (2.50±0.37)/cell, (7.01±1.97)μm2/cell respectively in the control group. PCNA labeling index was (36.87±14.51)% in the experimental group, and (52.24±10.86)% in the control group. There was significant difference in the expressions of AgNOR and PCNA between both the groups (P<0.05). Conclusion 125IUdR, which can incorporate into DNA of dividing tumor cells, can selectively kill the tumor cells in S-phase, significantly suppress the expressions of AgNOR and PCNA of C6 glioma cells, and inhibit the proliferation of C6 glioma cells.
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