摘要
目的 动态观察HepG2 细胞在顺铂压力下存活细胞中P53 、C myc、Bax、Bcl 2等的变化 ,进一步探讨HepG2 顺铂耐药的机制。方法 采用免疫组化法和RT PCR法测定在顺铂压力下存活HepG2 细胞内凋亡和抗凋亡因子P53 、C myc、Bax、Bcl 2、NF κB的变化。结果 在顺铂压力下存活HepG2 细胞P53 、C myc等凋亡相关因子无明显变化。Bcl 2持续升高 ,Bax逐渐下降 ,Bcl 2 /Bax的比率值呈进行性升高。NF κBmRNA在 7d后出现明显阳性。结论 在顺铂持续压力下HepG2细胞的存活机制与Bcl 2持续升高、Bax逐渐下降有关 ,NF
Objective To observe the dynamic changes of P 53 , C myc, Bax, Bcl 2, and NF κB in surviving HepG 2 cells under the continuous stress of cisplatin for the investigation of the potential role in the resistance of HepG 2 cells to cisplatin. Methods The apoptosis of HepG 2 cells and changes of the apoptosis associated factors including P 53 , C myc, Bax, Bcl 2, and NF κB in the surviving HepG 2 cells were detected by immunohistochemical and RT PCR assays. Results No obvious change of P 53 and C myc was found in the surviving HepG 2 cells under cisplatin stress, but persistent increase of Bcl 2 and decrease of Bax and a continuous increase of Bcl 2/Bax ratio were found. Markedly positive expression of NF κB mRNA was found at 7 d after the stress of cisplatin. Conclusion The mechanisms of the surviving HepG 2 cells under continuous stress of cisplatin may be associated with the increase in Bcl 2 and decrease in Bax, specially the continuous increase in Bcl 2/Bax ratio, while the positive NF κB mRNA expression may be associated with the later events after HepG 2 cell survive.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2004年第12期1116-1119,共4页
Journal of Third Military Medical University