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目的探讨PARP抑制剂BMN-673在替尼泊苷(VM-26)诱导的MG-63细胞增殖及凋亡中的作用。方法采用常规方法培养MG-63细胞,经BMN-673和(或)ABT-888处理12h后,采用MTT比色法分析细胞的活力,采用流式细胞术Annexin V-FITC/PI双染法分析细胞凋亡水平,采用ELISA试验与细胞中半胱氨酸蛋白酶活性。结果 BMN-673与VM-26联用组、对照组及VM-26单独使用组细胞活力分别为58.00%、97.00%和77.00%,差异有统计学意义(P<0.05);细胞凋亡水平分别为42.00%、3.00%和23.00%,差异有统计学意义(P<0.01);细胞中Caspase-3、Caspase-6和Caspase-9活性分别为12.15%、8.28%和9.09%,5.25%、2.51%和3.12%,2.89%、0和0.98%,差异有统计学意义(P<0.05)。结论 PARP抑制剂BMN-673可通过抑制PARP-1活性,进而抑制细胞DNA损伤修复,来增强MG-63细胞对抗癌药物VM-26的药敏性,为骨肉瘤化疗药物的临床研究了提供新的思路。
Objective To investigate the role of PARP inhibitor BMN-673 in the proliferation and apoptosis of MG-63 cells induced by teniposide (VM-26). Methods MG-63 cells were cultured by conventional method. After being treated with BMN-673 and / or ABT-888 for 12 hours, MTT colorimetric assay was used to analyze the viability of MG-63 cells. Flow cytometry was performed using Annexin V-FITC / PI double staining The level of apoptosis was measured by ELISA and cystatin activity in cells. Results The viability of BMN-673 and VM-26 groups were 58.00%, 97.00% and 77.00%, respectively, with statistical significance (P <0.05). The apoptosis rates of BMN-673 and VM- (P <0.01). The activities of Caspase-3, Caspase-6 and Caspase-9 in the cells were 12.15%, 8.28% and 9.09%, 5.25% and 2.51 % And 3.12%, 2.89%, 0 and 0.98% respectively, the difference was statistically significant (P <0.05). Conclusion PARP inhibitor BMN-673 can enhance the drug sensitivity of anti-cancer drug VM-26 in MG-63 cells by inhibiting the activity of PARP-1 and then repressing DNA damage. The clinical study of chemotherapy drugs for osteosarcoma New ideas.