长春新碱致神经病理性疼痛模型中胶质细胞及IL-1β、GDNF 表达的变化

 目的 研究长春新碱致神经病理性疼痛中胶质细胞是否活化及其作用机制。方法 大鼠腹腔内重复注射长春新碱建立模型。免疫组化检测脑及脊髓中星形胶质细胞和小胶质细胞特异性活化标志物GFAP和OX-42的表达。RT-PCR测定IL-1β和GDNF mRNA在脊髓腰段的表达。结果 给药大鼠分别在第8天和第5天出现机械痛闽降低和热痛耐受时间降低。给药大鼠中脑导水管周围灰质及脊髓灰质中见明显胶质细胞的活化。给药组较对照组IL-1β表达增加，GDNF表达减少。结论 胶质细胞在长春新碱致神经病理性疼痛中明显活化。IL-1β及GDNF与长春新碱引起的神经病理性疼痛有关。

Activation of Glial Cells and Expression Change of IL-1β, GDNF in Vincristine-induced Neuropathic Pain

Objective 　Glial cells play essential roles in creation and maintenance of pain state. This study was designed to explore the activation of glial cells in vincristine-induced neuropathic pain , and to find how glial cells influence pain threshold. Methods 　We adapted a model by using repeated int raperitoned injection of vincristine. By immunohistochchemical technique , the expression of specific activation markers of ast rocytes and microglials , glial fibrillary acidic protein ( GFAP) and OX-42 respectively , were examined in brain and lumbar intumescentia. Using RT-PCR analysis techniques , the expression of interleukine-1β( IL-1β) and glial cell line-derived neurot rophic factor ( GDNF) in lumbar intumescentia were tested. Results 　Mechanical hyperalgsia appeared on the 8th>>> day and thermal hyperalgsia appeared on the 5th>>> day of vincristine treatment . Glial cells were obviously active in periaquenductal gray and spinal gray.IL-1βexpression was increased in chemotherapy group , while GDNF was higher in control group. Conclusion 　Glial cells were active in Vincristine-induced neuropathic pain. The change of expression of IL-1βand GDNF were involved in neuropathic pain evoked by vincristine.