髓核致炎性神经痛大鼠背根神经节ASIC3表达相关性研究

Expression of Acid-sensing Ion Channel 3 in Dorsal Root Ganglion Cells in Rats with Inflammatory Radicular Pain Following Application of Nucleus Pulposus

【目的】观察髓核致炎后不同时期大鼠背根神经节(DRG)3型酸敏感离子通道(ASIC3)的表达,及其与痛敏形成的关系。【方法】将SD大鼠尾部髓核0.4mg移植于左侧腰5DRG而建立炎性神经痛动物模型,或术毕DRG周围给予ASIC3抑制剂阿米洛利0.1mg,用von-Fair细丝检测机械性痛敏阈值,观察DRG的ASIC3阳性细胞数,并检测不同时间点DRG的ASIC3蛋白表达。【结果】髓核移植后大鼠机械痛阈较术前持续降低(P<0.001),DRG上ASIC3阳性细胞数增多(P<0.05),术后第7天时表达至高峰(P<0.05);ASIC阻断剂阿米洛利可抑制模型鼠痛阈降低(P<0.001)。【结论】髓核移植使大鼠DRGASIC3表达增加,抑制ASIC3表达可减轻机械性痛敏,ASIC3上调可能是椎间盘突出致炎性神经痛的重要促进因素。

【Objective】 To Explore the expression of acid-sensing ion channel 3 （ASIC3） in dorsal root ganglion （DRG） cells of rats after application of nucleus pulposus,and its impact on mechanical pain threshold. 【Methods】 Inflammatory radicular pain of mature male rats was induced by application of nucleus pulposus about 0.4 mg on left lumbar 5 DRG. Mechanical pain threshold was tested with von Fair Hairs at different time points. Expression of ASIC3 protein was analyzed by immunofluorescent detection and Western blotting. 【Results】 The mechanical pain threshold was slided down rapidly and persistently following nucleus pulposus autografting （P 0.001）,combined with augment of ASIC3 immunoreactive DRG cells （P 0.05）. The expression of ASIC3 protein reached peak on postoperative day 7 （P 0.05）. The change of mechanical pain threshold and ASIC3 immunoreactive DRG cells were significantly inhibited by amiloride （P 0.001,P 0.01）. 【Conclusions】 The expression of ASIC3 in DRG was enhanced in rats following application of nucleus pulposus. Inflammatory radicular pain was reduced by inhibitor of ASIC3. The up-regulation of ASIC3 may facilitate the chronic radicular pain induced by disc herniation.