Electroacupuncture attenuates mechanical allodynia by suppressing the spinal JNK1/2 pathway in a rat model of inflammatory pain
Electroacupuncture attenuates mechanical allodynia by suppressing the spinal JNK1/2 pathway in a rat model of inflammatory pain
复制标题
DOI：
10.1016/j.brainresbull.2014.06.004
复制
发表时间：
2014-09-01
影响因子：
3.8
通讯作者：
Fang, Jun-Fan
中科院分区：
文献类型：
--
作者：
Du, Jun-Ying;Fang, Jian-Qiao;Fang, Jun-Fan
背景：电针对完全弗氏佐剂（CFA）诱导的炎性痛具有显著的镇痛作用。脊髓中c-Jun N-末端激酶1/2（JNK 1/2）信号转导通路的激活与炎性疼痛相关。然而，电针的镇痛作用与炎症痛中JNK 1/2信号转导通路的关系尚不清楚。在本研究中，我们使用建立的大鼠模型CFA诱导的炎性疼痛，探讨脊髓JNK 1/2通路在EA介导的alginancy.Results的作用：我们观察到的缩足阈值下降和增加在1和3天后，CFA注射到右后爪水肿。注射CFA 3天后，磷酸化c-Jun N-末端激酶1/2（p-JNK 1/2）蛋白及其下游靶点、转录调节因子p-c-Jun和激活蛋白-1（AP-1）以及环氧合酶-2（考克斯-2）和瞬时受体电位香草素1（TRPV 1）的表达上调。电针可明显减轻CFA引起的炎性疼痛。电针可降低CFA组大鼠脊髓背角p-JNK 1/2蛋白水平和考克斯-2 mRNA表达，下调p-c-Jun蛋白水平和AP-1 DNA结合活性，但对TRPV 1 mRNA表达无影响。此外，EA和JNK抑制剂SP 600125协同抑制CFA诱导的痛觉过敏和抑制考克斯-2 mRNA的表达在脊髓backhorn.Conclusions：我们的研究结果表明，EA减轻炎性疼痛的行为，至少部分，通过减少考克斯-2的表达在脊髓通过JNK 1/2信号通路。脊髓JNK 1/2信号转导通路的失活可能是电针抗炎性痛的潜在机制。(C)2014 Elsevier Inc. All rights reserved.
Background: Electroacupuncture (EA) has a substantial analgesic effect on inflammatory pain induced by complete Freund's adjuvant (CFA). The activation of the c-Jun N-terminal kinase 1/2 (JNK1/2) signal transduction pathway in the spinal cord is associated with inflammatory pain. However, the relationship between EA's analgesic effect and the JNK1/2 signal transduction pathway in the inflammatory pain remain unclear. In the present study, we used the established rat model of CFA-induced inflammatory pain to investigate the role of the spinal JNK1/2 pathway in EA-mediated analgesia.Results: We observed a decrease in paw withdrawal thresholds and an increase in paw edema at 1 and 3 days after injecting CFA into the right hindpaw. CFA, 3 days after injection, upregulated expression of phospho-c-Jun N-terminal kinase1/2 (p-JNK1/2) protein and its downstream targets, the transcriptional regulators p-c-Jun and activator protein-1 (AP-1), as well as cyclooxygenase-2 (COX-2) and the transient receptor potential vanilloid 1 (TRPV1). EA significantly alleviated CFA-induced inflammatory pain. In addition, EA reduced p-JNK1/2 protein levels and COX-2 mRNA expressions, a degree of down-regulated p-c-Jun protein level and AP-1 DNA binding activity in the spinal dorsal horn of CFA-administered animals, but it had no effect on TRPV1 mRNA expression. Furthermore, EA and the JNK inhibitor SP600125 synergistically inhibited CFA-induced hyperalgesia and suppressed the COX-2 mRNA expression in the spinal dorsal horn.Conclusions: Our findings indicate that EA alleviates inflammatory pain behavior, at least in part, by reducing COX-2 expression in the spinal cord via the JNK1/2 signaling pathway. Inactivation of the spinal JNK1/2 signal transduction pathway maybe the potential mechanism of EA's antinociception in the inflammatory pain model. (C) 2014 Elsevier Inc. All rights reserved.