一氧化氮在TRAIL诱导凋亡中对p53和VCP蛋白表达的影响  

THE INFLUENCE OF NITRIC OXIDE ON THE p53 AND VCP PROTEIN EXPRESSION IN THE PROCESS OF TRAIL- INDUCED APOPTOSIS SIGNAL PATHWAY

作　　者：安玲[1] 纵媛 吉栋德[1] 王荣华[3] 李正娥[4] 曹成珠[2] 苏占海[2] 

机构地区：[1]青海省人民医院 [2]青海大学医学院 [3]青海大学附属医院 [4]青海红十字医院

出　　处：《青海医学院学报》2015年第2期103-107,共5页Journal of Qinghai Medical College

基　　金：国家自然基金项目(81160259);青海省自然科学基金面上项目(2013-Z-907);青海省应用基础研究项目(2013-Z-726)

摘　　要：目的研究NO在TRAIL诱导凋亡过程中对p53和VCP蛋白表达的影响。方法利用Western blot蛋白印迹法检测各蛋白表达水平;用MTT方法检测细胞凋亡和caspase-3激酶激活状态。结果内源性NO表达产生的一氧化氮可提高TRAIL诱导的细胞凋亡率,同时增加caspase-3激酶激活活性。内源性NO对p53蛋白表达水平无影响,但是对VCP蛋白表达的上调有一定促进作用。结论内源性NO对管家基因p53蛋白无明显影响,但对与内质网压力相关的VCP蛋白有调节作用。Objective To investigate the influence of nitric oxide （NO） on the p53 and valosin - containing pro- tein （VCP） protein expression in the process of tumor necrosis factor - related apoptosis inducing ligand （TRAIL） mediated apoptosis signal pathway. Method Through Western blot to detect the protein expression. The cell apopto- sis and caspase - 3 activity were analyzed by MTT. Results Endogenous nitric oxide enhances the TRAIL - induced apoptosis level, and it also promoted caspase -3 activity. The p53 protein expression has not been effected by induc- ible nitric oxide synthase（iNOS） expression, but VCP protein expression can be increased by iNOS expression after induction. Conclusion Endogenous NO shows no influence on the p53 expression, but it regulates reticulum pressure -related protein VCP.

关 键 词：TRAIL INOS P53 VCP细胞凋亡 

分 类 号：R735[医药卫生—肿瘤]