抑制AQP4降低大鼠脊神经节ERK表达,减轻坐骨神经结扎导致神经病理性疼痛  

Inhibition of AQP4 alleviates neuropathic pain by sciatic nerve ligation via decrease of ERK expression in dorsal root ganglion in rat

作　　者：赵亮[1] 李丹[2] 刘囡[2] 刘璐 李洪鹏[2] ZHAO Liang;LI Dan;LIU Nan;LIU Lu;LI Hong-peng(Department of Bone Surgery,Shenyang No.5Hospital,Shenyang 110023;Department of Anatomy,College of Basic Medical Science,China Medical University,Shenyang 110122,China)

机构地区：[1]沈阳市第五人民医院骨外科,沈阳110023 [2]中国医科大学基础医学院解剖学教研室,沈阳110122

出　　处：《解剖科学进展》2018年第6期618-621,625,共5页Progress of Anatomical Sciences

基　　金：辽宁省教育厅重点项目(LZDK201704)

摘　　要：目的探讨AQP4抑制剂对坐骨神经结扎导致的神经病理性疼痛的作用及其可能机制。方法制作大鼠坐骨神经慢性压迫性损伤(CCI)模型,采用热痛刺激仪测量热痛感受性潜伏期,Western blot和免疫荧光(双重染色)方法检测ERK, JNK, p38表达。结果神经损伤可诱导ERK, JNK, p38信号分子表达及卫星胶质细胞活化,AQP4抑制剂TGN-020则削弱ERK,JNK和p38信号分子及卫星胶质细胞的活化;p-ERK和GFAP共表达的细胞在损伤后明显增多,TGN-020则显著降低这一表达。结论抑制AQP4减轻坐骨神经结扎导致的神经病理性疼痛与抑制神经节卫星胶质细胞活化和MAPK信号通路活化相关。Objective To investigate the effect and possible mechanism of AQP4 inhibitor on the neuropathic pain caused by lumbar disc herniation in rat. Methods The chronic constriction injury(CCI) model was established in rat. The thermal withdrawal latency was measured, the expression of ERK, JNK and p38 proteins was detected by Western blot and Immunofluorescence double staining. Results The nerve damage caused the upregulation of ERK, JNK and p38 molecules and the activation of satellite glial cells, but TGN-020(AQP4 inhibitor) weakened the expression of ERK, JNK, and p38 pathways and the activation of satellite glial cells. The number of p-ERK and GFAP positive cells increased obviously after injury, but reduced significantly by TGN-020. Conclusion The inhibition effect of AQP4 inhibitor on the neuropathic pain is related to the decrease of satellite glial cells activation and ERK signaling molecules expression in dorsal root ganglion.

关 键 词：坐骨神经损伤 卫星胶质细胞 AQP4 ERK信号通路 大鼠 

分 类 号：R747[医药卫生—神经病学与精神病学]