摘要
目的:研究莱菔硫烷对急性髓系白血病细胞株KG1a细胞凋亡的影响及作用机制。方法:利用细胞增殖实验CCK-8试剂盒检测SFN对KG1a细胞增殖的抑制作用,利用流式细胞术检测SFN对KG1a细胞早期凋亡率的影响,进一步利用PCR、Western-blot技术研究SFN对KG1a细胞Bax和bcl2 mRNA和蛋白水平表达的影响。结果:(1)SFN可抑制KG1a细胞的增殖,且随SFN浓度增加和作用时间延长抑制率增加;(2)在0,4,8,12μmol·L^(-1)SFN作用KG1a细胞后,其早期凋亡率呈浓度依赖性增加,早期凋亡率分别为0,3.12%,13.33%,28.18%;(3)SFN可增加KG1a细胞的Bax的mRNA和蛋白的表达,与对照组(0μmol·L^(-1)浓度组)存在统计学差异(P<0.05)。SFN可降低bcl2 mRNA和蛋白表达水平,12μmol·L^(-1)SFN浓度组的蛋白表达与对照组相比,差异有统计学意义(P<0.05)。结论:SFN可通过调控Bax和bcl2基因促进KG1a细胞凋亡,抑制KG1a细胞增殖。
OBJECTIVE To investigate the effect of sulforaphane on apoptosis of KG1 a cells and explore its relevant mechanism.METHODS CCK-8 assay was firstly used to investigate the inhibiting effects of sulforaphane on proliferation of KG1 a cells and screen out the appropriate drug concentration.Furthermore,the apoptosis rate of KG1 a cells was observed by FACs.The expression of Bax and bcl2 in KG1 a cells were affected by sulforaphane as analyzed by Reverse Transcription-Polymerase Chain Reaction and Western-blot.RESULTS Sulforaphane could inhibit the proliferation of KG1 a cells in a dose and time dependent manner.And the number of apoptosis cells in sulforaphane group was significantly greater than that in the control group.The early apoptosis rates were 0,3.12%,13.33% and 28.18% respectively in KG1 a cells treated by 0,4,8μmol and12μmol sulforaphane.Then,sulforaphane could increase the expression of Bax protein and mRNA levels in a dose dependent manner compared with control group（P〈0.05）.And 12μmol sulforaphane could down regulate bcl2 protein levels（P〈0.05）.CONCLUSION Sulforaphane can inhibit proliferation and promote apoptosis of KG1 a cells effectively.And then sulforaphane inhibits the proliferation of KG1 a cells through regulating the expression of Bax and bcl2,which may be related to the cell apoptosis.
出处
《中国医院药学杂志》
CAS
北大核心
2017年第9期826-829,共4页
Chinese Journal of Hospital Pharmacy
基金
教育部新世纪优秀人才支持计划(编号:NCET-13-0990)
河南省教育厅科学技术研究重点项目(编号:15A320009
13B320220)
新乡医学院培育基金项目(编号:2013QN119)
国家大学生创新训练项目(编号:201510472002)
