中文摘要：

【目的】 探讨肿瘤坏死因子α（TNF-α）激活的下游信号转导途径-核转录因子kappaB （NF-κB）、 JNK和p38 MAPK是否参与运动神经损伤引起的大鼠病理性疼痛的形成,并探讨其可能机制;【方法】 采用痛行为学测试和免疫荧光组织化学方法,观察鞘内注射NF-κB 抑制剂（PDTC）、 p38 MAPK 抑制剂（SB203580）和JNK 抑制剂（SP600125）对腰5脊神经前根切断（L5-VRT）大鼠机械性痛过敏及腰5背根神经节（DRG）内电压门控钠通道（Nav1.3）表达的影响; 【结果】 ①L5-VRT术前应用NF-κB抑制剂PDTC可完全抑制大鼠双侧机械性痛过敏的形成,并阻断同侧L5 DRG内Nav1.3的上调;②术前应用p38 MAPK抑制剂SB203580和JNK抑制剂SP600125主要抑制大鼠对侧后肢的机械性痛过敏;对手术同侧DRG内Nav1.3的表达,SB203580和SP600125分别具有完全阻断和部分阻断作用;③术后7 d给予PDTC或SB203580或SP600125对已形成的大鼠机械性痛过敏均无影响; 【结论】 运动神经损伤可能通过NF-κB、 p38 MAPK和JNK途径调控未损伤DRG神经元内Nav1.3的表达从而进一步调控L5-VRT引起的大鼠后肢机械性痛过敏.

英文摘要：

[Objective] To test the idea that the downstream molecules of TNF-α [NF-kappa B, p38 MAPK, and c-jun N- terminal kinase （JNK） ] might be involved in the development of neuropathic pain induced by L5 ventral root transection （L5- VRT）. [Method] The behavioral test and the method of immunofluorescence staining were used to observe the affections of the three inhibitors of NF-kappa B, p38 MAPK, and JNK on the mechanical allodynia induced by L5 VRT and the expression of Navl.3 in L5 dorsal root ganglion （DRG）. [Result] Intrathecal injection of NF-kappa B inhibitor （PDTC） or JNK inhibitor （SP600125） or p38 inhibitor （SB203580）, administered 10 rain before L5-VRT, all of these significantly inhibited the expression of Navl.3 in ipsilateral L5 DRGs. Single pre-treatment of PDTC completely attenuated bilateral mechanical allodynia. Intrathecal injection of SB203580 or SP600125 being applied 10 min before LS-VRT and once daily thereafter until day 7 after surgery, attenuated the contralateral, but not the ipsilateral, mechanical allodynia. [Conclusion] NF-κB, p38 MAPK, and JNK pathways, through down-regulating the expression of Nav1.3 in L5 DRG, could inhibit the rat mechanical allodynia induced by motor nerve injury.