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瘦素缺乏小鼠椎间盘退变的组织学观察

Histologic observation of intervertebral disc degeneration in lack-leptin mice

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【作者】 郭震李新锋戴力扬

【Author】 GUO Zhen,LI Xin-feng,DAI Li-yang.Department of Orthopaedics,Xinhua Hospital,Shanghai Jiao Tong University,Shanghai 200092,China

【机构】 上海交通大学医学院附属新华医院骨科

【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。

【Abstract】 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.

【关键词】 椎间盘免疫组织化学瘦素小鼠
【Key words】 Intervertebral discImmunohistochemistryLeptinMice
  • 【文献出处】 脊柱外科杂志 ,Journal of Spinal Surgery , 编辑部邮箱 ,2012年02期
  • 【分类号】R681.53
  • 【被引频次】1
  • 【下载频次】96
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