苯甲酰胺阻止N-甲基-N′-亚硝基氮亚硝基胍引起的神经胶质瘤细胞株凋亡  

Benzamide prevents glioma cell line from apoptosis induced by MNNG

作　　者：李刚[1] 王金环[1] 蔡宝立[1] 史国利[1] 

机构地区：[1]南开大学分子生物学研究所,天津300071

出　　处：《中国神经科学杂志》2000年第1期41-44,共4页

摘　　要：研究 DNA损伤所造成的神经胶质瘤细胞 TJ90 5凋亡过程中聚 ADP核糖基聚合酶 [poly( ADP-ribose) polymerase,PARP]的作用。用 N-甲基 - N′-亚硝基氮亚硝基胍 ( MNNG)和 PARP的 NAD位点特异性抑制剂苯甲酰胺 ( benzamide,BA) ,分别或同时处理神经胶质瘤细胞 TJ90 5。结果发现在 MNNG的作用下 ,细胞的增殖活性受到明显的抑制 ,细胞凋亡显著 ;单独用 BA处理细胞时 ,细胞的增殖活性及细胞的凋亡与对照组细胞相似。 BA和 MNNG共同处理下的 TJ90 5细胞的增殖活性和凋亡指数与对照组细胞及 BA组细胞相比均无明显差异。说明 PARP在诱导神经胶质瘤细胞凋亡方面起重要作用 ,该作用可被 PARP的特异性抑制剂所抑制。To study the function of poly (ADP ribose) polymerase in the apoptosis of glioma TJ905 caused by DNA damage, the cells were treated either by N methyl N′ nitro N nitrosogunidine (MNNG), or benzamide (BA), a special inhibitor of PARP, or the mixture of them. The results showed that under the induction of MNNG, the proliferation of TJ905 was inhibited definitely and TJ905 had definite apoptosis reaction. When treated by benzamide alone, TJ905's proliferation and apoptosis resembled the control. Nor did the mixture of BA and MNNG influence the proliferation and the apoptosis of TJ905. The results suggest that PARP plays an important role in inducing TJ905's apoptosis.

关 键 词：神经胶质瘤 细胞凋亡 苯甲酰胺 PARP 

分 类 号：R730.2[医药卫生—肿瘤]