节点文献

IL-1β诱导小鼠椎间盘软骨终板细胞炎性退变的细胞模型研究

Inflammatory disc degeneration cell model induced by IL-1β on mouse endplate chondrocytes

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 张宇赵永见周泉王拥军郑为超

【Author】 ZHANG Yu,ZHAO Yongjian,ZHOU Quan,WANG Yongjun,ZHENG Weichao Department of Immunology,Medical College,Anhui University of Science and Technology,Huainan 232001,China

【机构】 安徽理工大学医学院免疫学教研室上海中医药大学脊柱病研究所上海中医药大学附属龙华医院骨伤科

【摘要】 目的通过IL-1β体外诱导小鼠椎间盘软骨终板细胞建立退变细胞模型,并研究其作用机制。方法 10 ng/ml IL-1β诱导小鼠椎间盘软骨终板细胞24 h后,用cck-8法检测不同时间点IL-1β对软骨终板细胞增殖作用的影响,透射电镜观察细胞退变情况,细胞免疫荧光和Western blot检测细胞退变相关蛋白表达。结果诱导组细胞较正常组细胞增殖减慢,细胞肥大化比例增加,出现线粒体肿胀、核扭曲、染色质边集,染色质及胞质松散等细胞坏死及凋亡表现,且colⅡ、Aggrecan表达下降,colⅩ、MMP-1、MMP-3、MMP-13、TIMP-1表达增加。结论 IL-1β可诱导软骨终板细胞发生退变。

【Abstract】 We aimed to establish a disc degeneration cell model by IL-1β induction on mice endplate chondrocytes,and analyze its mechanism.Firstly,we induced the endplate chondrocytes with 10 ng/ml IL-1β for 24 h.Then we used cck-8 to measure the proliferation during the different times.After that,we observed cell degeneration by TEM,and tested the expression of cell degeneration-related protein through immunofluorescence and Western blot.The results showed that the proliferation rate of induced cells was decreased compared with normal ones.The proportion of hypertrophy cell in induced group was higher too.Besides,there were many markers of meronecrobiosis and apoptosis in induced cells such as mitochondrial swelling,nucleus distortion,chromatin margination,chromatin and streaming loose.Moreover,we found the protein expression of col Ⅱ and aggrecan decreased,but col Ⅹ,MMP-1,MMP-3,MMP-13,and TIMP-1 increased in induced group.We concluded that IL-1β can induce endplate chondrocytes to be degeneration.

【关键词】 IL-1β椎间盘软骨终板细胞退变
【Key words】 IL-1βIntervertebral discEndplate chondrocytesDegeneration
【基金】 国家自然科学基金(30901914,30801478,30701118);上海市优秀学科带头人计划(08XD1404000);上海市高校创新团队计划(沪教委科【2009】6号);安徽省自然科学基金项目(11040606M203);安徽高校省级自然科学研究重点项目(KJ2009A038);国家教育部高等学校博士点基金(20093107110003)
  • 【文献出处】 免疫学杂志 ,Immunological Journal , 编辑部邮箱 ,2012年08期
  • 【分类号】R-332
  • 【被引频次】27
  • 【下载频次】388
节点文献中: 

本文链接的文献网络图示:

本文的引文网络