白细胞介素-1β在病理性疼痛大鼠脊髓LTP中的作用及机制

Role of interleukin -1βin spinal LTP in rats with neuropathic pain

目的:探讨白细胞介素-1β(interleukin-1β,IL-1β)在神经病理性疼痛大鼠脊髓背角C纤维诱发电位长时程增强(long-term potentiation,LTP)中的作用及其机制。方法:用坐骨神经部分损伤(spared nerve iniury,SNI)和腰5前根切断(lumbar 5 ventral root transection,L5 VRT)方法复制大鼠病理性疼痛模型,观察外源性IL-1β对正常大鼠及病理性疼痛模型大鼠脊髓背角C纤维诱发电位的影响,并且检测p38 MAPK(p38 mitogen-activatedprotein kinase)和NF-κB(nuclear factor-kappa B)信号通路在其中的作用。结果:500μg/L IL-1β对正常大鼠C纤维介导的基本突触传递和高频刺激诱导的LTP都没有影响,而5μg/L的IL-1β可以在神经病理性疼痛模型的大鼠上诱导出LTP。预先用p38 MAPK或NF-κB的抑制剂(SB203580或PDTC)可以完全阻断IL-1β诱导的LTP。结论:外源性IL-1β可诱导神经病理性疼痛大鼠脊髓背角C纤维诱发电位的LTP。38 MAPK和NF-κB信号通路可能参与这一过程。

AIM：To investigate the role of interleukin-1β（IL-1β） in the long-term potentiation（LTP） of C -fiber-evoked field potentials in rats with neuropathic pain.METHODS：The rat model of neuropathic pain was produced by spared nerve injury（SNI） of sciatic nerve or the method of lumbar 5 ventral root transection（L5 VRT）.The effect of exogenous IL-1βon C-fiber-evoked field potentials of spinal dorsal horn was tested in both intact rats and the rats with neuropathic pain.The roles of p38 MAPK and NF -κB in the process were also evaluated.RESULTS：IL-1βat concentration of 500μg/L affected neither basal synaptic transmission mediated by C-fiber nor spinal LTP induced by high frequency stimulation in intact rats.However,low concentration（5μg/L） of IL-1βinduced LTP of C-fiber-evoked field potentials in the rats with neuropathic pain.Pretreatment with either p38 MAPK inhibitor（SB203580） or NF -κB inhibitor（PDTC） completely blocked LTP induced by IL-1β.CONCLUSION;Exogeneous IL-1βmight induce spinal LTP of C-fiber-evoked field potentials in the rats with neuropathic pain.p38 MAPK and NF -κB may be involved in the process.