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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 10μL作为治疗组,对照组则在左侧三叉神经根处注射生理盐水10μL,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。
Objective: To study the repair effect of GDNF on demyelination sites in the SD rat model of trigeminal neuralgia. Methods: Thirty successful SD rat models of trigeminal neuralgia were selected and divided into treatment group, control group and blank group. After anesthesia, the rats were fixed in a rat brain locator, and 10% of 2% GDNF was injected into the left trigeminal nerve root of the rats as a treatment group. In the control group, 10 L of normal saline was injected into the left trigeminal nerve roots, To deal with. The free trigeminal ganglion was dissected and GFAP immunofluorescence staining of astrocytes was performed to observe the changes of astrocytes between the experimental and control groups. Data were statistically analyzed using SPSS 13.0 software package. Results: At 3, 7, 14, 21 and 28 days after operation, the pain response of rats in the treatment group was slower than that in the control group, and the number of astrocytes in the trigeminal ganglion was significantly decreased compared with the control group. Conclusion: The increase of trigeminal neuralgia is associated with neurodegeneration and demyelinating lesions. GDNF can effectively participate in the regulation of hyperalgesia and may participate in the regulation of trigeminal neuralgia by promoting regeneration of nerve fibers.