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IL-6 contributes to Nav1.3 up-regulation in trigeminal nerve following chronic constriction injury.
Neurological Research ( IF 1.9 ) Pub Date : 2020-04-13 , DOI: 10.1080/01616412.2020.1747719 Ming-Xing Liu 1 , Jun Zhong 2 , Lei Xia 2 , Ning-Ning Dou 2 , Shi-Ting Li 2
Neurological Research ( IF 1.9 ) Pub Date : 2020-04-13 , DOI: 10.1080/01616412.2020.1747719 Ming-Xing Liu 1 , Jun Zhong 2 , Lei Xia 2 , Ning-Ning Dou 2 , Shi-Ting Li 2
Affiliation
Background: To verify the hypothesis that the nature of trigeminal neuralgia (TN) is an ectopic impulse induced by sodium channel modulated by cytokines, we conducted an animal study using the infraorbital nerve chronic constriction injury (CCI) model in rats.Method: The expression of Nav1.3 or IL-6 in the infraorbital nerve (ION) and trigeminal ganglion (TG) were detected by western blot and immunocytochemistry after administration of antisense oligodeoxynucleotide sequence (AS), IL-6 or Anti-IL-6.Results: With intrathecal administration of AS or mismatch oligodeoxynucleotide sequence (MM) in the CCI rats, the Nav1.3-IR in ION and TG accounted for 2.2 ± 0.51% and 8.5 ± 3.1% in AS+CCI group vs. 6.9 ± 1.3% and 38.7 ± 4.8% in MM+CCI group (p < 0.05), respectively. While with local administration of IL-6 in those with sham operation, it accounted for 7.4 ± 2.1% and 45.5 ± 3.4% in IL-6+ sham group vs. 1.9 ± 0.67% and 8.1 ± 1.3% in vehicle+sham group (p < 0.05); with local administration of anti-IL-6 in CCI rats, 4.5 ± 0.78% and 32.1 ± 9.6% in Anti-IL-6+ CCI group vs 8.9 ± 2.1% and 61.4 ± 11.2% in vehicle+CCI group (p < 0.05).Discussion: We believe that the emergence of Nav1.3 from the compressed trigeminal nerve might be an important structural basis for the development of the ectopic excitability on the axon and IL-6 may play a role of necessary precondition.
中文翻译:
IL-6有助于慢性收缩损伤后三叉神经中Nav1.3的上调。
背景:为了验证三叉神经痛(TN)的性质是由细胞因子调节的钠通道诱导的异位冲动的假说,我们使用大鼠眶下神经慢性收缩损伤(CCI)模型进行了动物研究。应用反义寡脱氧核苷酸序列(AS),IL-6或Anti-IL-6后,通过western blot和免疫细胞化学检测了眶下神经(ION)和三叉神经节(TG)中的Nav1.3或IL-6的含量。结果:通过鞘内注射AS或在CCI大鼠中错配寡聚脱氧核苷酸序列(MM),ION和TG中的Nav1.3-IR分别占AS + CCI组的2.2±0.51%和8.5±3.1%,而6.9±1.3%和MM + CCI组分别为38.7±4.8%(p <0.05)。在假手术患者中局部使用IL-6,IL-6 +假手术组占7.4±2.1%和45.5±3.4%,而媒介物+假手术组分别为1.9±0.67%和8.1±1.3%(p <0.05); 在CCI大鼠中局部施用抗IL-6,抗IL-6 + CCI组为4.5±0.78%和32.1±9.6%,而媒介物+ CCI组为8.9±2.1%和61.4±11.2%(p <0.05 )讨论:我们认为从压缩的三叉神经中出现Nav1.3可能是轴突上异位兴奋性发展的重要结构基础,而IL-6可能扮演了必要的前提条件。
更新日期:2020-04-13
中文翻译:
IL-6有助于慢性收缩损伤后三叉神经中Nav1.3的上调。
背景:为了验证三叉神经痛(TN)的性质是由细胞因子调节的钠通道诱导的异位冲动的假说,我们使用大鼠眶下神经慢性收缩损伤(CCI)模型进行了动物研究。应用反义寡脱氧核苷酸序列(AS),IL-6或Anti-IL-6后,通过western blot和免疫细胞化学检测了眶下神经(ION)和三叉神经节(TG)中的Nav1.3或IL-6的含量。结果:通过鞘内注射AS或在CCI大鼠中错配寡聚脱氧核苷酸序列(MM),ION和TG中的Nav1.3-IR分别占AS + CCI组的2.2±0.51%和8.5±3.1%,而6.9±1.3%和MM + CCI组分别为38.7±4.8%(p <0.05)。在假手术患者中局部使用IL-6,IL-6 +假手术组占7.4±2.1%和45.5±3.4%,而媒介物+假手术组分别为1.9±0.67%和8.1±1.3%(p <0.05); 在CCI大鼠中局部施用抗IL-6,抗IL-6 + CCI组为4.5±0.78%和32.1±9.6%,而媒介物+ CCI组为8.9±2.1%和61.4±11.2%(p <0.05 )讨论:我们认为从压缩的三叉神经中出现Nav1.3可能是轴突上异位兴奋性发展的重要结构基础,而IL-6可能扮演了必要的前提条件。