期刊文献+

促红细胞生成素对大鼠急性脊髓损伤后核因子κB及炎症因子表达的影响 被引量:6

Effects of erythropoietin on the expression of NF-κB and inflammatory cytokines after acute spinal cord injury in rats
原文传递
导出
摘要 目的观察促红细胞生成素(EPO)对大鼠急性脊髓损伤后脊髓组织核因子κB(NF-κB)表达及肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)、IL-6水平的影响,探讨其减轻急性脊髓损伤后继发性脊髓损伤的机制。方法 18只SD大鼠随机均分为对照组、损伤组和治疗组,用动脉瘤夹从两侧夹闭脊髓30 s造成脊髓损伤模型。治疗组分别予术后1 h和1、2、3 d腹腔注射EPO 5000U/kg。术后3 d处死大鼠取材,用EMSA法检测脊髓组织中NF-κB活性,ELISA法检测TNF-α、IL-1β、IL-6表达。结果治疗组脊髓组织中NF-κB、TNF-α、IL-1β、IL-6的水平均比损伤组显著降低(P<0.05)。结论 EPO能下调急性脊髓损伤后脊髓组织中炎症因子的表达,从而抑制炎症反应,对继发性脊髓损伤有一定的保护作用。 Objective To observe the influence of erythropoietin(EPO) on the expressions of nuclear factor-kappa B(NF-κB) and inflammatory factors of tumor necrosis factor-α(TNF-α),interleukin(IL)-1β and IL-6 following acute spinal cord injury and to explore the possible mechanism of reducing secondary spinal cord injury.Methods Eighteen SD rats were randomly and equally divided into 3 groups of sham control group,injury model group and treatment group.Treatment group was given intraperitoneal injection of EPO(5000U/kg) at 1h,on the 1st,2nd and 3rd day after establisgment of spinal cord injury model.All rats were sacrificed after 3 days.The expression of NF-κB was detected by EMSA assay and the expressions of TNF-α,IL-1β and IL-6 were examined with ELISA.Results The levels of NF-κB,TNF-α,IL-1β,IL-6 in spinal cord tissue of treatment group were significantly lower than those in injury model group(P0.05).Conclusion EPO administration can down-regulate the expressions of the inflammatory factors,inhibit the inflammatory response and play a role in protecting the secondary spinal cord injury.
出处 《江苏医药》 CAS CSCD 北大核心 2011年第4期381-383,共3页 Jiangsu Medical Journal
关键词 脊髓损伤 促红细胞生成素 Spinal cord injury Erythropoietin
  • 相关文献

参考文献11

二级参考文献43

  • 1羊明智,吴叶,章亚东,侯树勋,贾连顺.钙离子及其阻滞剂对脊髓灰质c-fos基因表达的影响[J].中华创伤骨科杂志,2005,7(2):137-140. 被引量:8
  • 2李想,王少波.脊髓损伤后炎症性细胞因子表达的变化及甲基强的松龙的影响[J].中国康复理论与实践,2005,11(2):91-93. 被引量:10
  • 3Mautes AE, Weinzierl MR, Donovan F, et al. Vascular events after spinal cord injury: contribution to secondary pathogenesis [ J ]. Phys Ther,2000,80 ( 7 ) :673 - 687. 被引量:1
  • 4Xu W, Chi L, XU R, et al. Increased production of reactive oxygen species contributes to motor neuron death in a compression mouse model of spinal cord injury [ J ]. Spinal Cord, 2005,43 ( 4 ) : 204 - 213. 被引量:1
  • 5Yune TY, Lee SM, Kim SJ, et ah Manganese superoxide dismutase induced by TNF-beta is regulated transcriptionally by NF-kappaB after spinal cord injury in rats [ J ]. Neurotrauma, 2004,21 ( 12 ) : 1778-1794 被引量:1
  • 6Toborek M, Malecki A, Garrido R, et al. Arachidonic acid - induced oxidative injury to cultured spinal cord neurons [ J]. Neurochem, 1999,73 (2) :684 - 692. 被引量:1
  • 7Bethea JR, Castro M, Keane RW, et al. Tranmatic spinal cord injury induces nuclear factor-kappaB activation [ J ]. Neurosci, 1998, 18(9) :3251 -3260. 被引量:1
  • 8Jimenez Garza O, Camacho J, Ibarra A, et al. Early effects of modulating nuclear factor-kappaB activation on traumatic spinal cord injury in rats[ J]. Ann N Y Acad Sci,2005,1053:148 -150. 被引量:1
  • 9La Rosa G, Cardali S, Genovese T, et al. Inhibition of the nuclear factor-kappaB activation with pyrrolidine dithiocarbamate attenuating inflammation and oxidative stress after experimental spinal cord trauma in rats [ J ]. Neurosurg Spine,2004,1 ( 3 ) :311 - 321. 被引量:1
  • 10Sen R, Baltimore D. Multiple nuclear factors interact with the immunoglobulin enhancer sequences [ J 1. Cell, 1986,46 ( 5 ) : 705 - 716. 被引量:1

共引文献20

同被引文献118

引证文献6

二级引证文献115

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部