NF-κB在右美托咪定抑制利多卡因神经毒性中的作用

发布时间：2018-05-04 04:43

本文选题：核转录因子-κB + 利多卡因　；参考：《中国现代医学杂志》2017年23期

【摘要】：目的探讨核转录因子-κB(NF-κB)在右美托咪定(Dex)抑制利多卡因对坐骨神经分支损伤(SNI)模型大鼠脊髓神经毒性中作用。方法取40只SD雄性大鼠,随机分为5组:健康对照组(C组)、SNI模型组(S组)、SNI利多卡因组(SL组)、SNI利多卡因+Dex组(SLD组)、SNI利多卡因+Dex+NF-κB阻断剂组(SLDB组),每组8只大鼠。所有大鼠行硬膜外置管,C组未做其他处理。在疼痛稳定后,S组鞘内注射生理盐水20μl,SL组鞘内注射10%利多卡因20μl,SLD组在SL组基础上腹腔注射75μg/kg Dex,SLDB组在SLD组基础上鞘内注射40μg吡咯烷二硫代氨基甲酸酯。连续药物处理7 d后取各组大鼠L4~6节段脊髓,透射电镜观察脊髓形态;末端标记法荧光染色观察脊髓背角细胞凋亡;Western blot检测Bax和Caspase-1表达量;酶联免疫吸附法检测各组脊髓匀浆液中TNF-α和IL-1β的表达。结果 (1)与S组比较,SL组、SLD组及SLDB组的机械痛阈值升高,细胞凋亡数、Bax、Caspase-1、TNF-α及IL-1β表达增加(P0.05);(2)与SL组比较,SLD组和SLDB组细胞凋亡数、Bax、Caspase-1、TNF-α及IL-1β表达降低(P0.05);(3)与SLD组比较,SLDB组细胞凋亡数、Bax、Caspase-1、TNF-α及IL-1β表达增加(P0.05)。结论 Dex抑制利多卡因对SNI模型大鼠脊髓神经毒性可能与激活NF-κB通路、抑制炎症及凋亡有关。
[Abstract]:Objective to investigate the role of nuclear transcription factor-魏 B (NF-魏 B) in inhibiting the neurotoxicity of lidocaine on spinal cord in rats with sciatic nerve branch injury (SNI). Methods Forty Sprague-Dawley male rats were randomly divided into 5 groups: normal control group (group C) and control group (n = 8): group S (n = 8) treated with lidocaine group (n = 8) and group S (n = 8) treated with lidocaine Dex group (n = 8). All rats were treated with epidural catheterization without any other treatment. After stable pain, intrathecal injection of 10% lidocaine (10%) lidocaine 20 渭 l / L SLD group (S group) was injected intrathecally into the SLD group (40 渭 g) of pyrrolidine dithiocarbamate (40 渭 g), and 75 渭 g/kg Dexanine SLDB group was injected intrathecally on the basis of SL group, and 40 渭 g pyrrolidine dithiocarbamate was injected intrathecally on the basis of SLD. The morphology of spinal cord was observed by transmission electron microscope (TEM), and the expression of Bax and Caspase-1 in spinal dorsal horn cell apoptosis was detected by fluorescence staining with end labeling method. The expression of TNF- 伪 and IL-1 尾 in spinal cord homogenate was detected by enzyme-linked immunosorbent assay (Elisa). Results compared with S group, the mechanical pain threshold of SL group and SLDB group was higher than that of S group. Compared with SL group and SLDB group, the expression of Baxia Caspase-1 TNF- 伪 and IL-1 尾 decreased (P0.05TNF- 伪 and IL-1 尾 expression decreased) compared with SLD group, the expression of BaxCaspase-1TNF- 伪 and IL-1 尾 increased P0.05a and P0.05a in SLD group and SLD group were significantly higher than that in SLD group (P < 0.05), and the expression of BaxCaspase-1TNF- 伪 and IL-1 尾 in SLD group was significantly higher than that in SLD group (P < 0.05). Conclusion the inhibitory effect of Dex on the neurotoxicity of lidocaine on spinal cord in SNI model rats may be related to the activation of NF- 魏 B pathway and the inhibition of inflammation and apoptosis.
【作者单位】：广西省百色市人民医院麻醉科;广西医科大学第二附属医院疼痛科;
【基金】：广西自然科学基金(No:2013GXNSFAA019137)
【分类号】：R614

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