前炎性细胞因子白细胞介素1β和肿瘤坏死因子在保留神经损伤所致机械性痛敏发生中的不同作用(英文)

Different roles of pro-inflammatory cytokines interleukin-1 beta and tumor necrosis factor in mechanical hyperalgesia induced by spared nerve injury in rats

背景:脊髓胶质细胞的激活参与了保留神经损伤(sparednerveinjury,SNI)诱致的机械性痛敏的发生。脊髓胶质细胞激活释放的前炎性细胞因子在这个过程中是否扮演了重要的角色。目的:探讨了白细胞介素1(interleukin-1,IL-1)和肿瘤坏死因子(tumornecrosisfactor,TNF)在SNI诱致的机械性痛敏中的不同作用。设计:随机对照试验。地点和对象:解放军第四军医大学实验动物中心提供的40只健康成年雄性Sprague-Dawley大鼠。干预:实验分两组:实验组:鞘内分别给予白细胞介素-1受体拮抗剂(interleukin-1receptorantagonist,IL-1ra),肿瘤坏死因子抗血清(tumornecrosisfactoranti-serum,anti-TNF)和同时给予IL-1ra和anti-TNF。对照组:鞘内给予相应的溶媒。术前和术后分别检测大鼠后爪机械性刺激阈值。主要观察指标:大鼠检测机械性刺激缩足阈值。结果:①鞘内给予IL-1ra可以对大鼠单侧后爪内侧和外侧在术后1周内产生一个明显的对机械性痛敏的抑制,而anti-TNF没有这样的作用。②同时鞘内给予IL-1ra和anti-TNF可以产生更加明显的机械性痛敏抑制,抑制作用可以长达术后6周。结论:脊髓胶质细胞激活释放的前炎性细胞因子IL-1和TNF在SNI诱致的机械性痛敏中扮演了重要的角色。IL-1和TNF在SNI诱致的机械性痛敏中的作用不同。

BACKGROUND:The activation of spinal cord glia contributes to mechanical hypera lgesia induced by spared nerve injury(SNI).Whether induced proinflammatory cytok ines play an important role during the process is unclear. OBJECTIVE:To investigate the different role of interleukin-1(IL-1) and tumor necrosis factor(TNF) in SNI-induced mechanical hyperalgesia. DESIGN:Randomized controlled study. SETTING and PARTICIPTANTS:Forty adult male Sprague-Dawley rats were provided by Experimental Animal Center of Fourth Military Medical University. INTERVENTION:The rats were divided into two groups:Intrathecal administrations of interleukin-1 receptor antagonist(IL-1ra),tumor necrosis factor anti-seru m(anti-TNF), and both were performed in the experimental group;As controls,the vehicle was intrathecally administrated.The paw withdrawal threshold to mechanic al stimulation was determined before and after operation. MAIN OUTCOME MEASURES:The paw withdrawal threshold to mechanical stimulation. RESULTS:①Intrathecal administrations of IL-1ra produced a significant inhibi tion of mechanical hyperalgesia in the medial and lateral part of the ipsialtera l hind paw over 1 week postoperatively,whereas the same treatment with anti-TNF had no effect.②Intrathecal administrations of both IL-1ra and anti-TNF resul ted in a more remarkable inhibition of mechanical hyperalgesia,and the inhibitor y effect extended to 6 weeks after operation. CONCLUSIONS:These data suggest that the releases of pro-inflammatory cytokine s IL-1 beta and TNF alpha by the activation of spinal cord glia may contribute to mechanical hyperalgesia induced by SNI,and pro-inflammatory cytokines IL-1 beta and TNF play a different role in the process.