摘要
[目的]探讨NF-κB信号通路在椎间盘退变中的激活机制及其作用。[方法]按照Pfirrmann椎间盘退变分级系统对患者进行分级,分别收集2012～2013年上海市第一人民医院手术患者的正常和退变椎间盘组织（退变102例,正常9例）,生化检测试剂盒测定椎间盘组织中丙二醛（MDA）、髓过氧化物酶（MPO）含量;凝胶迁移试验（EMSA）检测细胞核内NF-κB蛋白结合活性;RT-PCR和Western blotting检测凋亡相关分子CHOP和Caspase-3表达。[结果]椎间盘退变组织中MDA、MPO水平较正常对照组明显增加;EMSA显示髓核细胞核中NF-κB活性增高;RT-PCR和Western blotting结果显示椎间盘退变组织中凋亡相关分子CHOP和Caspase-3水平明显增高。[结论]髓核细胞受氧化应激作用后可通过激活NF-κB通路导致细胞凋亡从而在椎间盘退变中发挥作用。
[Objective] To study the relationship between nuclear factor- kappa B （NF- KB） signaling pathway and in- tervertebral disc degeneration. [ Methods] A total of 102 samples of degenerated lumbar intervertebral disc and 9 of normal in- tervertebral disc were obtained by surgery between 2012 and 2013 in Shanghai First People＇ s Hospital. The levels of malondial- dehyde （MDA） and myeloperoxidase （MPO） were detected using biochemistry colorimetry while the activity of NF - κB was de- termined using electrophoretic mobility shift assay （EMSA） . Cell apoptosis related molecules, including CHOP and caspase- 3, were measured using western blot and RT - PCR. [ Results] The levels of MDA and MPO were significantly higher in the intervertebral disc degeneration group than in the control group. Moreover, cell apoptosis related molecules （including CHOP and caspase - 3 ） and the activity of NF - κB were in- creased in the intervertebral disc degeneration group. [ Conclu- sion] We hypothesize that nucleus pulposus ceils are affected by oxidative stress and apoptosis occurs through the activation of the NF - κB pathway, which in turn plays a critical role in inter- vertebral disc degeneration.
出处
《中国矫形外科杂志》
CAS
CSCD
北大核心
2015年第5期458-462,共5页
Orthopedic Journal of China
基金
上海市科委生药领域科技项目(编号:11441900101)
关键词
NF-ΚB
椎间盘退变
氧化应激
细胞凋亡
NF - κB
intervertebral disc degeneration
oxidative stress
apoptosis
