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首页> 外文期刊>CNS neuroscience & therapeutics. >Electroacupuncture Suppresses Mechanical Allodynia and Nuclear Factor Kappa B Signaling in Streptozotocin‐Induced Diabetic Rats
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Electroacupuncture Suppresses Mechanical Allodynia and Nuclear Factor Kappa B Signaling in Streptozotocin‐Induced Diabetic Rats

机译：电针抑制链脲佐菌素诱导的糖尿病大鼠的机械异常性疼痛和核因子κB信号传导。

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Summary Aims To investigate whether electroacupuncture ( EA ) produced analgesic effect and whether nuclear factor kappa B ( NF ‐κ B ) and cystathionine β synthase ( CBS ) involved in EA ‐mediated analgesia in painful diabetic neuropathy in rats. Methods Diabetes was induced by an intraperitoneal injection of streptozotocin ( STZ ) in adult female rats. Mechanical pain threshold was measured by von Frey filaments. EA was applied at acupoint Z u‐ S an‐ L i ( ST ‐36) in both hindlimbs. Western blot analysis was employed to detect changes in protein levels of NF ‐κB and CBS in spinal dorsal root ganglion ( DRG s). Results Mechanical allodynia was developed 2 weeks after STZ injection and lasted for another 4 weeks. STZ injection significantly enhanced expression of p65 and CBS in lumbar L 4‐6 DRG s when compared with age‐matched controls. EA markedly attenuated mechanical allodynia. Importantly, EA treatment remarkably inhibited p65 and CBS expression in DRG s. Additionally, intrathecal injection of the p65 antagonist pyrrolidine dithiocarbamate attenuated mechanical allodynia and markedly inhibited CBS expression in DRG s in STZ rats. Conclusions These data indicate that EA produced an analgesic effect, which might be mediated at least in a part by inhibition of NF ‐κB signaling pathway in primary sensory neurons in rats with diabetes.
机译：概述目的研究电针（EA）是否产生镇痛作用，以及核因子κB（NFκB）和胱硫醚β合酶（CBS）是否参与EA介导的大鼠糖尿病性糖尿病神经痛镇痛。方法腹腔注射链脲佐菌素（STZ）致成年雌性大鼠糖尿病。机械疼痛阈值由冯·弗雷丝（von Frey）细丝测量。 EA在两个后肢的Z u‐S an‐L i（ST‐36）穴位上使用。蛋白质印迹分析用于检测脊髓背根神经节（DRG s）中NFκB和CBS蛋白质水平的变化。结果STZ注射后2周出现机械性异常性疼痛，并持续了4周。与年龄匹配的对照组相比，STZ注射显着增强了腰L 4-6 DRG s中p65和CBS的表达。 EA明显减轻了机械性异常性疼痛。重要的是，EA处理显着抑制了DRG中p65和CBS的表达。此外，鞘内注射p65拮抗剂吡咯烷二硫代氨基甲酸酯可减轻STZ大鼠DRG中的机械异常性疼痛，并显着抑制CBS表达。结论这些数据表明，EA具有镇痛作用，其作用可能至少部分是通过抑制糖尿病大鼠初级感觉神经元中的NFκB信号通路来实现的。

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