目的 通过定量检测加巴喷丁(GBP)对长春新碱(VCR)致神经病理性疼痛小鼠大脑皮层脑啡肽(ENK)的表达水平,探讨VCR致神经病理性疼痛发生机制及GBP防治神经病理性疼痛的相关脑皮层机制.方法 采用荧光定量PCR和酶联免疫分析方法 (ELISA),从两个水平分别检测VCR致痛组(V组)、GBP治疗组(C组)、GBP对照组(G组)和生理盐水对照组(N组)小鼠大脑皮层ENK的表达;同时检测小鼠热痛阈值变化情况及观察小鼠坐骨神经在光镜和电镜下组织形态和超微结构.结果 V组的坐骨神经在电镜下截面极不规则,髓鞘增粗且髓鞘板层质地疏松,颜色变浅,部分见严重病变处呈灶性溶解坏死.荧光定量PCR检测结果 显示,V组与N组比较,ENK表达水平差异无统计学意义;C组与V组比较,ENK表达水平差异也无统计学意义.结论 VCR致神经病理性疼痛的机制与原发的轴索变性和继发的脱髓鞘有关,与大脑皮层ENK含量变化无关;GBP防治VCR致神经病理性疼痛的镇痛机制与大脑皮层ENK的表达无相关性.%Objective To evaluate the role of cortical enkephalin in vincristine - induced neuropathic pain in mice, thus to assure the mechanism of gabapentin in prevention of neuropathic pain. Methods The cortical enkephalin expression in vincristine - induced pain group ( Group V ), gabapentin treatment group ( Group C ), gabapentin control ( Group G ) and saline control group ( Group N ) were assessed with RT - PCR and ELISA. Meanwhile, the thermal pain threshold and morphologic observation of sciatic nerve under light and electron microscopy were also recorded. Results An irregular shaped cross - section with thickened, loose texture and stainless myelin, scattered with necrosis lesions was observed in Group V. No significant difference in enkephalin expression was revealed between Group V and Group N or Group C. Conclusion The primary axonal degeneration and secondary demyelination are involved in vincristine - induced neuropathic pain, with no correlation with cortical enkephalin, which is not involved in the gabapentin prevention of vincristine - induced neuropathic pain.
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