期刊文献+

瘦素缺乏小鼠椎间盘退变的组织学观察 被引量:1

Histologic observation of intervertebral disc degeneration in lack-leptin mice
下载PDF
导出
摘要 目的探讨瘦素在椎间盘退变中的可能作用。方法采用HE染色观察6月龄雄性ob/ob小鼠(瘦素缺乏小鼠)和野生型小鼠(C57BL小鼠)椎间盘的形态学;免疫组织化学检测Ⅱ型胶原、蛋白聚糖的表达;Real-time PCR检测Ⅱ型胶原、Ⅹ型胶原及蛋白聚糖的基因表达。结果与野生型小鼠相比,ob/ob小鼠椎间盘HE染色表现为椎间盘组织的胶原结构紊乱、髓核碎裂、椎间盘高度降低,免疫组化检测显示Ⅱ型胶原、蛋白聚糖表达减少,Real-time PCR检测显示Ⅱ型胶原、蛋白聚糖基因表达下调而Ⅹ型胶原基因表达上调,差异有统计学意义(P<0.05)。结论活体内瘦素缺乏可能加速小鼠椎间盘退变。 Objective To explore the possible role of leptin in intervertebral disc degeneration.Methods The intervertebral discs of 6-month-old male ob/ob mice(lack-leptin mice) and wild type mice(C57BL mice) were histologically observed by HE staining.The expression of collagen Ⅱ and aggrecan were detected by immunohistochemistry.And the gene expression of collagen Ⅱ,collagen Ⅹ and aggrecan were measured by Real-time PCR.Results HE staining results showed collagen disorders,fragmentation of nucleus pulposus,and decreased height of intervertebral disc in ob/ob mice.Compare with the wild type mice,there were decreased protein level of collagen Ⅱ and aggrecan,downregulated mRNA expression of collagen Ⅱ and aggrecan,and upregulated mRNA expression of collagen Ⅹ in ob/ob mice.There was significant difference of the changes between wild type mice and ob/ob mice(P<0.05).Conclusion In vivo,lack of leptin may accelerate intervertebral disc degeneration in mice.
出处 《脊柱外科杂志》 2012年第2期113-117,共5页 Journal of Spinal Surgery
关键词 椎间盘 免疫组织化学 瘦素 小鼠 Intervertebral disc Immunohistochemistry Leptin Mice
  • 相关文献

参考文献3

二级参考文献14

  • 1[1]Maeda S,Kokubun S.Changes with age in proteoglycan synthesis in cells cultured in vitro from the inner and outer rabbit annulus fibrosus.Responses to interleukin-1 and interleukin-1 receptor antagonist protein.Spine,2000,25:166-169
  • 2[2]Murata Y,Onda A,Rydevik B,et al.Distribution and appearance of tumor necrosis factor-alpha in the dorsal root ganglion exposed to experimental disc herniation in rats.Spine,2004,29:2235-2241
  • 3[3]Weiler C,Nerlich AG,Bachmeier BE,et al.Expression and distribution of tumor necrosis factor alpha in human lumbar intervertebral discs:a study in surgical specimen and autopsy controls.Spine,2005,30:44-53
  • 4[4]Yoshida M,Nakamura T,Sei A,et al.Intervertebral disc cells produce tumor necrosis factor alpha,interleukin -1beta,and monocyte chemoattractant protein-1 immediately after herniation:an experimental study using a new hernia model.Spine,2005,30:55-61
  • 5[5]Solovieva S,Kouhia S,Leino-Arjas P,et al.Interleukin 1 polymorphismsand intervertebral disc degeneration.Epidemiology,2004,15:626 -633
  • 6[6]Rannou F,Corvol MT,Hudry C,et al.Sensitivity of anulus fibrosus cells to interleukin 1 beta.Comparison with articular chondrocytes.Spine,2000,25:17-23
  • 7[7]Adams MA,Freeman BJ,Morrison HP,et al.Mechanical initiation of intervertebral disc degeneration.Spine,2000,25:1625-1636
  • 8[8]Arend WP.The balance between IL-1 and IL-1 Ra in disease.Cytokine Growth Factor Rev,2002,13:323 -340
  • 9[9]Elenkov IJ,Chrousos GP.Stress hormones,proinflammatory and antiinflammatory cytokines,and autoimmunity.Ann N Y Acad Sci,2002,966:290-303
  • 10[10]Tsuzaki M,Guyton G,Garrett W,et al.IL-1 beta induces COX2,MMP-1,-3 and-13,ADAMTS -4,IL-1 beta and IL -6 in human tendon cells.J Orthop Res,2003,21:256 -264

共引文献31

引证文献1

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部