摘要
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。
AIM To observe the effect of Bcl-2 ribozyme on SMMC 7721 cells and to investigate bcl-2 inhibition of cellular apoptosis.METHODS PMTr-neo (sense Bcl-2 ribozyme eucaryotic expression vector) was introduced into SMMC7221 cells by using lipofectin mediation; TUNEL and TRAP were used in combination of ELISA and IHC to determine SMMC7721/ PMTr-neo proliferation and apoptosis. RESULTS Compared with the control, SMMC7721/ PMTr-neo presented a significant drop in bcl-2 expression, accompanied by remarkable apoptosis and telomerase activity decline.CONCLUSION Bcl-2 ribozyme promotes apoptosis of SMMC7721 cells and reduces telomerase activity. This provides a theoretical basis for applying antisense technique to treatment of hepatocarcinoma.
出处
《世界华人消化杂志》
CAS
2000年第4期417-419,共3页
World Chinese Journal of Digestology
关键词
肝肿瘤
BCL-2
核酶
细胞凋亡
liver neoplasms
Bcl-2
ribozyme
apoptosis
SMMC 7721
