摘要
目的探讨阿霉素对大鼠心肌细胞H9C2凋亡的影响及Krppel样因子4过表达对阿霉素所致H9C2细胞凋亡的影响。方法采用台盼蓝染色检测细胞存活率,流式细胞术检测细胞凋亡率,采用Western blotting检测Krppel样因子4及凋亡相关基因多聚二磷酸腺苷核糖聚合酶的表达。结果阿霉素能够诱导H9C2细胞凋亡,采用5μmol/L阿霉素处理时,24h变化最为明显;Krppel样因子4过表达之后,细胞凋亡率较转空载体组更高,达87.90%。阿霉素能够诱导Krppel样因子4在H9C2细胞中表达增加;Krppel样因子4过表达组多聚二磷酸腺苷核糖聚合酶裂解片段的表达水平明显上调。结论 Krppel样因子4能够促进阿霉素诱导的大鼠心肌细胞H9C2凋亡,其作用机制与多聚二磷酸腺苷核糖聚合酶有关。
Aim To investigate the effect of Krüppel-like factor 4（KLF4）overexpression on doxorubicin-induced apoptosis of rat myocardiocytes H9C2.Methods Trypan blue staining and cytometry were applied to detect apoptosis;Western blotting was applied to determine expressions of KLF4 and apoptosis-related gene poly ADP-ribose polymerase（PARP）.Results Trypan blue staining and cytometry results showed that doxorubicin could induce apoptosis of H9C2,and the apoptosis rate in KLF4-overexpression group was much higher than that of vector control group,which was 87.90%.Western blotting results showed that doxorubicin treatment could promote KLF4 expression in H9C2 cells,and the expression of PARP fragment was also up-regulated dramatically in KLF4-overexpression group.Conclusion KLF4 could promote doxorubicin-induced apoptosis of H9C2 cells,which potential mechanism may be involved with PARP.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2010年第3期181-183,共3页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金(30900623)
湖南省科技计划(2009FJ3169)基金资助
