背根神经节中IL-1β对神经病理性疼痛作用及其机制

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[关键词] 神经疼痛;白细胞介素1 ;丝裂原活化蛋白激酶14;脑源性神经营养因子[中图分类号] R745 [文献标志码][文章编号] 2096-5532（2025）02-0176-05

[Abstract] Objective ⋅1β （IL-1β）on the p38 mitogen-activated protein kinase（p38 MAPK）andbrain-derivedneurotrophicfactor（BDNF）signalingpathwaysinthedorsalrotganglia（DRG）ofmicewithspared nerveinjury（SNI）ofthesciaticnerve. Methods A mousemodelofSNIwasestablished，andthesham-operationgroupwasestablishedasacontrol.VonFreyfilamentswereusedtomeasurethemechanicalwithdrawalthreshold（MWT）ofmiceondays1， 3，5，7，10，and14afterSNIsurgery;quantitativePCRwasusedtomeasurethemRNAexpresionlevelof IL–Iβ ;Westernblot wasusedtomeasuretheproteinexpresionlevelsofphosphorylatedp38MAPK（p-p38MAPK），totalp38MAPK（t-p38MAPK）， andBDNFintheDRGondays7and14aftersurgery.ThemiceweregivenintrathecalinjectionoftheIL- 1β inhibitorIL-1Raand thep38 MAPKinhibitorSB203580to measure MWTandtheexpresionlevelsofIL- ⋅1β ，p-p38MAPK，andBDNF. Results Comparedwiththesham-operationgroup，theSNIgrouphadasignificantreductionin MWT F=12.51-22.75，P<0.01⟩ ）and significantincreasesinthemRNAexpresionlevelof IL–Iβ andtheproteinexpresionlevelsofp-p38MAPKandBDNFondays7 and14aftersurgery （F=8.56-52.69，P<0.05） ）.ComparedwiththeSNIgroup，theSNI+IL-1ragrouphadsignificantreductions intheproteinexpresionlevelsofp-p38 MAPKandBDNF F=8.56-52.69，P<0.05; ）andasignificantincreasein MWT t= 2.43，8.80，P<0.01） ）ondays7and14aftersurgery，andthe SNI+SB203580 grouphadasignificantreductionintheproteinexpresionlevelofBDNF （F=12.75，52.69，P<0.01） ）andasignificantincreasein MWT t=3.14，5.16，P<0.05⟩ ）. Conclusion Inhibitionof IL-1β canregulatethep38MAPKandBDNFsignalingpathways，therebyaleviatingneuropathicpaininducedbySNI.

[Keywords] neuralgia;interleukin-1beta;mitogen-activatedproteinkinase14;brain-derivedneurotrophicfactor

在2020年，神经病性疼痛被定义为“一种不愉快的感觉和情感体验，与实际或潜在的组织损伤有关”[1]。（剩余9693字）