摘要
目的在建立C6/Wistar胶质瘤大鼠模型的基础上,研究125IUdR介导俄歇电子释放对大鼠C6胶质瘤DNA靶点放疗后的肿瘤细胞凋亡。方法建立C6/Wistar胶质瘤大鼠模型后,应用流式细胞仪检测研究C6胶质瘤细胞的增殖动力学指标。结果实验组肿瘤细胞的S期百分比与对照组相比显著降低(P<0.001),G2+M期的细胞也随之减少,肿瘤细胞大量停滞在G0/G1期。实验组增殖指数明显低于对照组(P<0.001),而凋亡指数则显著增加(P<0.001)。结论125IUdR通过电离作用导致G1期细胞增殖阻滞及DNA断裂、诱导肿瘤细胞凋亡。
Objective To investigate the action and mechanism of Auger electron emitting from ^125IUdR on DNA - targeting radiotherapy of C6 glioma in rat based on establishment of a C6/Wistar glioma model. Methods A total of 50 male Wistar rats were randomizedly divided into three groups: Experimental group (n =20), Control group (n =20) and Sham group (n = 10) . The animals of two former groups were scpartcd into two subgroups: 5 day sacrificing group and survival analysis group. Experimental group were infused intracerebrallyJ25iUdR per 8 hour during proliferation peak (0. 2mCi/10μl/time) , total dosage is 0. 6mCi/rat. Control group were infused intracerebrally ^127IUdR per 8 hour (5. 6μm/10μl/time), total dosage was 16. 8μm/rat. Sham group were infused with 10μl of 0. 9% saline. Flow cytometric analysis was performed. Results 1. Gross pathological examination demonstrated tumor weight and diameter in experimental group were lower than control group ( P 〈 0.05 ) . 2. S phase fraction in experimental group decreased more than control group in flow cytometric analysis (P 〈0. 001 ) , cells in G2 + M phase also decreased, and tumor cells were blocked in G0/G1 phase. Proliferation index in experimental group was lower than control ( P 〈 0. 001 ) , but apoptosis index was higher ( P 〈 0. 001 ) . Conclusion ^125IUdR can lead to the inhibition of G1 stage cell multiplication and DNA breakage, induce tumor cell apoptosis by electrolytic dissociation.
出处
《云南医药》
CAS
2006年第3期200-202,共3页
Medicine and Pharmacy of Yunnan
基金
云南省自然科学基金资助项目(NO.1999CO112M)