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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:

21卷

期数:

2015年03期

页码:

35-38

栏目:

临床医学

出版日期:

2015-05-20

文章信息/Info

Title:

JNK signaling pathway in disc tissue of injury-extrusion type of lumbar disc herniation

文章编号:

1006-8147（2015）0-0035-04

作者:

李鹏飞¹;  马信龙² ; 王 涛² ; 田 鹏²; 韩 超²; 臧加成²; 孔敬波²

(1.天津医科大学总医院骨科,天津 300052; 2.天津市天津医院骨科研究所生物力学室,天津300211)

Author(s):

LI Peng-fei¹;  MA Xin-long²;  WANG Tao²;  TIAN Peng²;  HAN Chao²;  ZANG Jia-cheng²;  KONG Jing-bo²

(1.Department of Orthopaedics, General Hospital ,Tianjin Medical University, Tianjin 300052, China; 2.Biomechanics Laboratory of Orthopaedic Research Institute of Tianjin Hospital, Tianjin 300211, China)

关键词:

腰椎; 椎间盘移位; JNK信号通路

Keywords:

lumbar vertebrae;  intervertebral disk displacement;  JNK signaling pathway

分类号:

R681.5+3

DOI:

-

文献标志码:

A

摘要:

 目的：探究c-Jun氨基末端激酶（JNK）信号通路在腰椎损伤疝出型椎间盘组织中激活情况。方法：随机选择24例行手术治疗的腰椎间盘突出症（LDH）患者，其中12例损伤疝出型和12例退变突出型，分别为损伤疝出组和退变突出组。收集术中摘除的椎间盘组织，HE染色观察髓核组织病理变化；TUNEL染色分析髓核细胞凋亡情况；免疫蛋白印迹技术检测MKK4、JNK、pJNK、JunD蛋白表达水平。结果：损伤疝出组出现炎性细胞浸润的比例、髓核细胞凋亡计数以及MKK4、JNK、pJNK、JunD蛋白表达水平高于退变突出组（P<0.05）。结论：损伤疝出型髓核组织炎症反应更明显；JNK信号通路异常激活与髓核细胞凋亡增加可能是损伤疝出型LDH病理机制之一；JNK信号通路激活可能是LDH病理分型的标志之一。

Abstract:

Objective: To investigate the function of c-Jun N-terminal kinase (JNK) signaling pathway in disc tissue of injury-extrusion type lumbar disc herniation. Methods: Twenty four cases with lumbar disc herniation(LDH) were randomly chosen, of which 12 cases were injury-extrusion type (injury-extrusion group) and 12 cases were degeneration- protrusion type (degeneration- protrusion group). Disc tissue was collected (加上)during operation, and the pathological changes of nucleus pulposus tissue with HE staining were observed; the apoptosis of nucleus pulposus cells with TUNEL staining were analyzed; the expression levels of MKK4, JNK, pJNK, JunD protein with Western blotting were detected. Results: The proportion of inflammatory cells infiltration, the count of nucleus pulposus cells apoptosis and the expression levels of MKK4, JNK, pJNK, JunD protein of injury-extrusion group were significantly higher than degeneration- protrusion group(P<0.05). Conclusion: Local inflammation of nucleus pulposus tissue for injury-extrusion group is more significant; Abnormal activation of JNK signaling pathway and increase of nucleus pulposus cells apoptosis may be the pathological mechanism for injury-extrusion type of LDH; Abnormal activation of JNK signaling pathway may be a marker for pathological classification of LDH.

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相似文献/References:

[1]李鹏飞,马信龙,王 涛,等.腰椎损伤疝出型椎间盘组织JNK信号通路激活情况的研究[J].天津医科大学学报,2015,21(03):35.
　LI Peng-fei,MA Xin-long,WANG Tao,et al.JNK signaling pathway in disc tissue of injury-extrusion type of lumbar disc herniation[J].Journal of Tianjin Medical University,2015,21(03):35.
[2]李鹏飞,马信龙,王 涛,等.腰椎损伤疝出型椎间盘组织JNK信号通路激活情况的研究[J].天津医科大学学报,2015,21(03):35.
　LI Peng-fei,MA Xin-long,WANG Tao,et al.JNK signaling pathway in disc tissue of injury-extrusion type of lumbar disc herniation[J].Journal of Tianjin Medical University,2015,21(03):35.
[3]李鹏飞,马信龙 *,王 涛,等. 腰椎损伤疝出型椎间盘组织JNK信号通路激活情况的研究[J].天津医科大学学报,2015,21(01):35.
　LI Peng-fei,MA Xin-long,WANG Tao,et al.JNK signaling pathway in disc tissue of injury-extrusion type of lumbar disc herniation[J].Journal of Tianjin Medical University,2015,21(03):35.

备注/Memo

备注/Memo:

基金项目 天津市科技支撑重点项目（13ZCZDSY01700）

作者简介 李鹏飞（1987-），男，硕士在读，研究方向：脊柱外科；通信作者：马信龙，Email: maxinlong86@163.com。

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更新日期/Last Update: 2015-01-22