蛋白激酶C/NF-κB在X线辐射诱导HepG2细胞凋亡中的作用  

Antiapoptotic role of protein kinase C/nuclear factor κB induced by X-ray radiation in HepG2 cells

作　　者：孙爱民[1] 陈龙华[1] 刘英[1] 夏琼[1] 袁亚维[1] 

机构地区：[1]南方医科大学南方医院,广东广州510515

出　　处：《山东医药》2008年第27期24-26,共3页Shandong Medical Journal

基　　金：国家自然科学基金资助项目(39870809);广东省医学科学技术研究基金(WSTJJ20061112432325197210030046)。

摘　　要：目的探讨蛋白激酶C/核因子κB(NF-κB)在X线电离辐射诱导HepG2细胞凋亡中的作用。方法分对照组、辐射组、PMA(蛋白激酶C激活剂)组、SP(蛋白激酶C抑制剂)组。流式细胞仪检测细胞凋亡率;EM-SA检测NF-κB的激活。免疫印迹法检测IκB的表达。结果对照组、辐射组、PMA组、SP组细胞凋亡率分别为1.73%、20.90%、3.20%、40.57%。对照组的NF-κB微弱激活,辐射组NF-kB明显激活,并诱导了胞质内IκB的降解;PMA可增强NF-κB的激活,加强胞质内IκB的降解;SP减弱NF-κB的激活,抑制质内IκB降解。结论蛋白激酶C可能参与了6 Gy X线辐射诱导的HepG2细胞凋亡的保护机制,发挥抗凋亡作用,且可能是通过激活NF-κB来实现的。Objective To investigate the antiapoptotic role of protein kinase C/nuclear factor κB （NF-κB） induced by X-ray radiation in HepG2 cells. Methods Cells were divided into four groups： control group, radiation group, PMA group, SP group. Apoptosis rates of ceils were estimated by flow cytometry. EMSA technique was used to detect activation of NF-κB in HepG2 cells. Western blotting was used to assess expressions of phospho-IκB. Results Apoptosis rates in control, radiation group, PMA group and SP group were 1.73%, 20.90%, 3.20% and 40.57% respectively. NF-κB activation in control was slight and was increased gradually after X-ray radiated. PMA promoted nuclear factor-κB activation induced by X-ray radiation. On the contrary, SP played an opposite role in NF-κB activation. Moreover, degradation of cytoplasm IκB was showed by western blotting and PMA upregulated IκB degradation, SP downregulated it. Conclusion Protein kinase C/NF-κB is involved in protecting mechanism in radiation-induced apoptosis in HepG2 cells and is playing an antiapoptic role in X-ray radiated HepG2 cells.

关 键 词：电离辐射 蛋白激酶C NF—κB 凋亡 

分 类 号：R812[医药卫生—放射医学]