白细胞介素-1β在病理性疼痛大鼠脊髓LTP中的作用及机制

摘要

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 injury,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-activated protein kinase)和NF-κB (nuclear factor-kappa B)信号通路在其中的作用.结果:500 μg/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5 μg/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.p38 MAPK和NF-κB信号通路可能参与这一过程.%AIM: To invesligale lhe role of inlerleukin - 1β (IL - 1(3) in lhe long - Lerm polenlialion ( LTP) of C - fiber - evoked field polenlials in rals wilh neuropalhic pain. METHODS: The ral model of neuropalhic pain was produced by spared nerve injury ( SNI) of scialic nerve or lhe melhod of lumbar 5 venlral rool Iranseclion ( L5 VRT). The effecl of exogenous IL - 1 (3 on C - fiber - evoked field polenlials of spinal dorsal horn was lesled in bolh inlacl rals and lhe rals wilh neuropalhic pain. The roles of p38 MAPK and NF - kB in lhe process were also evaluated. RESULTS; IL - 1(3 al concentration of 500μg/L affecled neilher basal synaplic Iransmission medialed by C -fiber nor spinal LTP induced by high frequency slimulalion in inlacl rals. However, low concenlralion (5μg/L) of IL - 1β induced LTP of C - fiber - e-voked field polenlials in lhe rals wilh neuropalhic pain. Prelrealmenl wilh eilher p38 MAPK inhibitor (SB203580) or NF - kB inhibitor (PDTC) completely blocked LTP induced by IL - 1(3. CONCLUSION; Exogeneous IL - 1(3 mighl induce spinal LTP of C - fiber - evoked field polenlials in lhe rats wilh neuropathic pain. P38 MAPK and NF - kB may be involved in lhe process.