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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 investigate the role of poly ADP-ribose polymerase (PARP) in the apoptosis of glioma TJ905 cells induced by DNA damage. Glioma cells TJ905 were treated with N-methyl-N’-nitroso-nitrosoguanidine (MNNG) and NAD site-specific inhibitor benzamide (BA) . The results showed that under the action of MNNG, the proliferation activity of cells was obviously inhibited and apoptosis was remarkable. When treated with BA alone, the proliferation activity and apoptosis of cells were similar to that of the control group. The proliferative activity and apoptosis index of TJ905 cells treated with BA and MNNG had no significant difference compared with those of control cells and BA cells. Indicating that PARP plays an important role in inducing glioma cell apoptosis and this effect can be inhibited by PARP specific inhibitors.