Electroacupuncture improves allodynia and central sensitization via modulation of microglial activation associated P2X4R and inflammation in a rat model of migraine

作者全名：Zhou, Min; Pang, Fang; Liao, Dongmei; Yang, Yunhao; Wang, Ying; Yang, Zhuxin; He, Xinlu; Tang, Chenglin

作者地址：[Zhou, Min] Chongqing Tradit Chinese Med Hosp, Affiliated Hosp Chongqing Coll Tradit Chinese Med, Chongqing, Peoples R China; [Zhou, Min; Pang, Fang; Liao, Dongmei; Yang, Yunhao; Yang, Zhuxin; He, Xinlu] Chongqing Med Univ, Coll Tradit Chinese Med, Chongqing, Peoples R China; [Wang, Ying; Tang, Chenglin] Chongqing Coll Tradit Chinese Med, 61 Puguobao Rd,Bicheng St, Chongqing 402760, Peoples R China

通信作者：Tang, CL (通讯作者)，Chongqing Coll Tradit Chinese Med, 61 Puguobao Rd,Bicheng St, Chongqing 402760, Peoples R China.

来源：MOLECULAR PAIN

ESI学科分类：NEUROSCIENCE & BEHAVIOR

WOS号：WOS:001235774500001

JCR分区：Q2

影响因子：2.8

年份：2024

卷号：20

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：Electroacupuncture; migraine; microglial activation; central sensitization; allodynia; inflammation

摘要：Background: Recent studies have demonstrated that activated microglia were involved in the pathogenesis of central sensitization characterized by cutaneous allodynia in migraine. Activation of microglia is accompanied by increased expression of its receptors and release of inflammatory mediators. Acupuncture and its developed electroacupuncture (EA) have been recommended as an alternative therapy for migraine and are widely used for relieving migraine-associated pain. However, it remains rare studies that show whether EA exerts anti-migraine effects via inhibiting microglial activation related to a release of microglial receptors and the inflammatory pathway. Therefore, this study aimed to investigate EA' ability to ameliorate central sensitization via modulation of microglial activation, microglial receptor, and inflammatory response using a rat model of migraine induced by repeated epidural chemical stimulation. Methods: In the present study, a rat model of migraine was established by epidural repeated inflammatory soup (IS) stimulation and treated with EA at Fengchi (GB20) and Yanglingquan (GB34) and acupuncture at sham-acupoints. Pain hypersensitivity was further determined by measuring the mechanical withdrawal threshold using the von-Frey filament. The changes in c-Fos and ionized calcium binding adaptor molecule 1 (Ibal-1) labeled microglia in the trigeminal nucleus caudalis (TNC) were examined by immunflurescence to assess the central sensitization and whether accompanied with microglia activation. In addition, the expression of Ibal-1, microglial purinoceptor P2X4, and its associated inflammatory signaling pathway mediators, including interleukin (IL)-1 beta, NOD-like receptor protein 3 (NLRP3), and Caspase-1 in the TNC were investigated by western blot and real-time polymerase chain reaction analysis. Results: Allodynia increased of c-Fos, and activated microglia were observed after repeated IS stimulation. EA alleviated the decrease in mechanical withdrawal thresholds, reduced the activation of c-Fos and microglia labeled with Ibal-1, downregulated the level of microglial purinoceptor P2X4, and limited the inflammatory response (NLRP3/Caspase-1/IL-1 beta signaling pathway) in the TNC of migraine rat model. Conclusions: Our results indicate that the anti-hyperalgesia effects of EA ameliorate central sensitization in IS-induced migraine by regulating microglial activation related to P2X4R and NLRP3/IL-1 beta inflammatory pathway.

基金机构：Chongqing Yuzhong District Science and Technology Plan Project

基金资助正文：No Statement Available