中国口腔颌面外科杂志 ›› 2016, Vol. 14 ›› Issue (6): 495-498.

• 论著 • 上一篇    下一篇

GDNF在修复SD大鼠模型脱髓鞘位点中的作用

朱冰洁, 郭永峰, 李明子, 周青   

  1. 中国医科大学附属口腔医院 口腔颌面外科,辽宁省口腔医学研究所,辽宁省口腔疾病重点实验室,辽宁省口腔疾病转化医学研究中心,辽宁 沈阳 110002
  • 收稿日期:2015-11-23 修回日期:2016-05-05 出版日期:2016-11-20 发布日期:2016-12-05
  • 通讯作者: 周青,E-mail:zqapollo@163.com
  • 作者简介:朱冰洁(1989-),女,在读硕士研究生,E-mail:soloice0927@163.com

The role of glial cell line-derived neurotrophic factor (GDNF) in repair of demyelination in SD rat model with trigeminal neuralgia

ZHU Bing-jie, GUO Yong-feng, LI Ming-zi, ZHOU Qing   

  1. Department of Oral and Maxillofacial of Stomatology, China Medical University; Liaoning Institute of Dental Research. Shenyang 110002, Liaoning Province, China
  • Received:2015-11-23 Revised:2016-05-05 Online:2016-11-20 Published:2016-12-05

摘要: 目的 研究GDNF对三叉神经痛SD大鼠模型中脱髓鞘位点的修复作用。方法 选取30只已经建立成功的SD大鼠三叉神经痛模型,分为治疗组、治疗对照组以及空白组。麻醉后,将大鼠固定在大鼠脑定位仪上,向大鼠左侧三叉神经根注射2% GDNF 10 μL作为治疗组,对照组则在左侧三叉神经根处注射生理盐水10 μL,空白组不予处理。解剖游离大鼠三叉神经节,行星形胶质细胞GFAP免疫荧光染色,观察星形胶质细胞在实验组和对照组之间的变化。采用SPSS 13.0 软件包对数据进行统计学分析。结果 术后3、7、14、21、28 d,治疗组大鼠较对照组对疼痛反应刺激迟钝,三叉神经节内星形角质细胞较治疗对照组显著减少。结论 三叉神经痛病变多与神经变性、脱髓鞘病变有关。GDNF能够有效参与痛觉过敏的调控过程,并可能通过促进神经纤维修复再生,参与调控三叉神经痛。

关键词: 三叉神经痛, GDNF, 髓鞘再生

Abstract: PURPOSE: To discuss the role of glial cell line-derived neurotrophic factor (GDNF) in repair of demyelination in SD rat model with trigeminal neuralgia. METHODS: Thirty SD rat model with trigeminal neuralgia had been successfully established and were divided into the treatment group, control group and blank group. The rats were fixed on the rat brain locator after anesthesia. 10 μL 2% GDNF was injected in the left trigeminal nerve root in the treatment group. 10 μL normal saline solution was injected at the same area in the control group. Planetary astrocyte GFAP immunofluorescence staining was performed to observe the changes of astrocytes in the treatment group 、control group and bland group. SPSS 13.0 software package was used for statistical analyzed. RESULTS: 3,7,14,21,28 days after operation, rats in the treatment group was not sensitive to pain stimulus than the control group and the blank group. Keratinocyte in the treatment group was significantly reduced compared with those in control and blank group. CONCLUSIONS: Trigeminal neuralgia is associated with nerve degeneration and demyelination. GDNF can effectively participate in the regulation of pain, and may be involved in the regulation of trigeminal neuralgia by promoting repair and regeneration of nerve fibers.

Key words: Trigeminal Neuralgia, GDNF, Remyelination

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