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大鼠坐骨神经损伤后脊髓运动神经元凋亡及其机制研究 被引量:4

Research of apoptosis and mechanism of dynamoneure following sciatic nerves injury in rats
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摘要 目的探讨大鼠坐骨神经损伤后雪旺细胞(schwann cells,SCs)中核因子-κB(nuclear factor-kappa B,NF-κB)的表达及其对脊髓运动神经元凋亡的调控作用。方法健康成年雄性SD大鼠36只,体重200~250g,随机分为正常对照组(n=-6)和坐骨神经钳夹损伤组(n=30)。采用免疫组化、计算机图像分析技术,对正常和损伤后不同时间1、3、7、14及21d的坐骨神经SCs中NF—κB的表达进行检测。同时取与坐骨神经相连的L4~L6段脊髓作原位末端标记技术(TUNEL)检测脊髓运动神经元的凋亡。结果与正常对照组相比较,损伤组坐骨神经SCs中NF—κB的表达显著改变,其变化趋势为先升高后降低,伤后3d达高峰。随后逐渐下降,21d接近正常值;损伤组脊髓运动神经元凋亡数在损伤后表现出相同的变化趋势。相关分析表明两者呈显著正相关。结论坐骨神经损伤后脊髓运动神经元发生不同程度的凋亡,SCs中NF—κB可能参与这种凋亡的调控过程。 [Objective] To explore the expression of nuclear factor-kappa B (NF-κB) in schwann cells (SCs) and its effect on motor neuron apoptosis following sciatic nerves injury in adult rats. [Methods] 36 healthy adult male SD rats were divided randomly into normal control group (n =6) and crushing group (n =30). The expression of NF-κB of normal and injury nerves in SCs indifferent days (1, 3, 7, 14 and 21 days) were examined by immunohistochemical technique and the motor neuron apoptosis were investigated by TUNEI. Both were quantitateed by image analysis. [Results] In crushing group, the expression of NF-κB was markedly higher than that in the normal control group. At 1 day after crushing NF-κB was raised, reached peak at 3 days, and recovered at 21 days. The same trend was observed in the time-course on motor neuron apoptosis after sciatic nerves injury. Correlation analyses revealed that motor neuron apoptosis was significantly and positively correlated with the expression of NF-κB. [Conclusions] After injury of sciatic nerves, the presence and up-regulation of NF-κB in SCs may be involved in motor neuron apoptosis.
出处 《中国现代医学杂志》 CAS CSCD 北大核心 2007年第10期1169-1172,共4页 China Journal of Modern Medicine
基金 创伤 烧伤与复合伤国家重点实验室开放课题基金(NO.2006A-3) 重庆市自然科学基金(NO.2004CC35)
关键词 坐骨神经 核因子-ΚB 运动神经元 凋亡 sciatic nerves injury nuclear factor-kappa B motor neuron apoptosis
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  • 1[1]Wanner GA, Muller P, Ertel W et al. Differential effect of cyclooxygenase metabolites on proinflammatory cytokine release by Kupffer cells after liver ischemia and reperfusion [J]. Am J Surg, 1998; 175(2): 146.
  • 2[2]Steinberg P, Lafranconi WM, Wolf CR et al. Xenobiotic metabolizing enzymes are not restricted to parenchymal cells in rat liver [J]. Mol Pharmacol,1987; 32 (4): 463.
  • 3[3]Zhou D, Chen S. Characterization of a silencer element in the human aromatase gene [J]. Arch Biochem Biophys, 1998; 353 (2): 213.
  • 4[4]Jufferson KK, Smith MF Jr, Bobak DA. Role of intracellular calcium and NF-κB in the clostridium difficile toxin A-induced up-regulation and secretion of IL-8 from human monocytes [J].J Immunol, 1999; 163 (10): 5183.
  • 5[6]Van Bossuyt H, Wisse E. Cultured Kupffer cells, isolated from human and rat liver biopsies, ingest endotoxins [J]. J Hepatol,1988; 7(1): 45.
  • 6[8]Biffl WI, Moore EE, Moore FA et al. Interleukin-6 in the injured patient: marker of injury or mediator of inflammation [J].Ann Surg, 1996; 224 (5): 647.
  • 7[10]Tran-Thi TA, Decker K, Baeuerle PA. Differential activation of transcription factors NF-κB and AP-1 in rat liver macrophage[J]. Hepatology, 1995; 22(2): 613.
  • 8Barbacid M. The Trk family of neurotrophin receptor. J Neurobiol, 1994; 25(11):1386-1403.
  • 9Pliego- Rivero FB, Bayatti N,Giannakoulopoulos X, et al. Brain -derived neurotrophic factor in human platelets. Biochem Pharmacol,1997; 54(1): 207-209.
  • 10Zhou XF, Chie ET, Deng YS, et al. Injured primary sensory neurons switch phenotype for brain- derived neurotrophic factor in the rat. Neuroscience, 1999; 92(3): 841-853.

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