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目的 观察Bcl-2核酶对SMMC-7721细胞的作用,探讨bcl-2抑制细胞凋亡的机制。 方法 经脂质体介导的方法将PMTr-neo(正向Bcl-2核酶真核表达载体)导入SMMC 7721细胞中,细胞克隆转移扩大培养后,采用TUNEL,TRAP结合ELISA流式细胞仪,免疫组化技术检测SMMC 7721/PMTr-neo细胞增殖及细胞凋亡。 结果 较对照组SMMC 7721/PMTr-neo细胞bcl-2表达水平显著下降,伴有显著细胞凋亡现象及端粒酶活性下降。 结论 Bcl-2核酶可促进SMMC 7721细胞发生凋亡,并降低细胞端粒酶活性,为反义技术在肝癌治疗中应用提供理论依据。
Objective To observe the effect of Bcl-2 ribozyme on SMMC-7721 cells and to explore the mechanism of bcl-2 inhibiting apoptosis. Methods PMTr-neo (positive Bcl-2 ribozyme eukaryotic expression vector) was transfected into SMMC 7721 cells by liposome-mediated method. After the cell clones were expanded and cultured, TUNEL and TRAP combined with ELISA were used to detect the expression of PMTr- Immunohistochemistry was used to detect cell proliferation and apoptosis in SMMC 7721 / PMTr-neo cells. Results Compared with control group, the expression of bcl-2 in SMMC 7721 / PMTr-neo cells was significantly decreased, with significant apoptosis and decreased telomerase activity. Conclusion Bcl-2 ribozyme can promote the apoptosis of SMMC 7721 cells and decrease the telomerase activity, providing a theoretical basis for the application of antisense technology in the treatment of hepatocellular carcinoma.