Electroacupuncture Suppresses Mechanical Allodynia and Nuclear Factor Kappa B Signaling in Streptozotocin-Induced Diabetic Rats
Electroacupuncture Suppresses Mechanical Allodynia and Nuclear Factor Kappa B Signaling in Streptozotocin-Induced Diabetic Rats
复制标题
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 Kappa B 信号传导
DOI：
10.1111/cns.12035
复制
发表时间：
2013-02-01
影响因子：
5.5
通讯作者：
Xu, Guang-Yin
中科院分区：
文献类型：
--
作者：
Shi, Lei;Zhang, Hong-Hong;Xu, Guang-Yin
目的探讨电针对糖尿病痛性神经病变大鼠的镇痛作用及核因子-κ β（NF-κ B B）和胱硫醚β合酶（CBS）是否参与电针镇痛作用。方法用链脲佐菌素（STZ）腹腔注射建立成年雌性大鼠糖尿病模型。用von Frey细丝法测定机械痛阈。电针治疗组采用电针双侧足三里穴。Western blot检测脊髓背根神经节（dorsal root ganglion，DRG）NF-κ B B和CBS蛋白表达的变化。结果STZ注射后2周出现机械性痛觉超敏，并持续4周。与年龄匹配的对照组相比，STZ注射显著增强了腰椎L4-6 DRG中p65和CBS的表达。电针可明显减轻机械性痛觉超敏。更重要的是，电针治疗显著抑制背根神经节中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衰减机械异常性疼痛，并显着抑制CBS在STZ大鼠DRG的表达。结论电针对糖尿病大鼠的镇痛作用可能与抑制NF-κ B B信号通路有关。
Aims To investigate whether electroacupuncture (EA) produced analgesic effect and whether nuclear factor kappa beta (NF-kappa B) and cystathionine beta 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 Zu-San-Li (ST-36) in both hindlimbs. Western blot analysis was employed to detect changes in protein levels of NF-kappa B and CBS in spinal dorsal root ganglion (DRGs). Results Mechanical allodynia was developed 2weeks after STZ injection and lasted for another 4weeks. STZ injection significantly enhanced expression of p65 and CBS in lumbar L4-6 DRGs when compared with age-matched controls. EA markedly attenuated mechanical allodynia. Importantly, EA treatment remarkably inhibited p65 and CBS expression in DRGs. Additionally, intrathecal injection of the p65 antagonist pyrrolidine dithiocarbamate attenuated mechanical allodynia and markedly inhibited CBS expression in DRGs 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-kappa B signaling pathway in primary sensory neurons in rats with diabetes.