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Effects of Electroacupuncture on the Regulation of Chemokine Induced Spinal Activation of Microglia in the Rat Model of Neuropathic Pain

흰쥐 신경병증성 통증 모델에서 전침이 케모카인이 유도하는 척수 교세포 활성화 조절에 미치는 영향

  • Sindhuri, Vishnumolakala (Department of Korean Medical Science, School of Korean Medicine, Pusan National University) ;
  • Lee, Ji Eun (Korean Medicine Research Center for Healthy Aging, Pusan National University) ;
  • Park, Hye-Ji (Korean Medicine Research Center for Healthy Aging, Pusan National University) ;
  • Kim, So-Hee (Korean Medicine Research Center for Healthy Aging, Pusan National University) ;
  • Koo, Sungtae (Department of Korean Medical Science, School of Korean Medicine, Pusan National University)
  • 비슈누몰라칼라 신드후리 (부산대학교 한의학전문대학원 한의과학과) ;
  • 이지은 (부산대학교 건강노화한의과학연구센터) ;
  • 박혜지 (부산대학교 건강노화한의과학연구센터) ;
  • 김소희 (부산대학교 건강노화한의과학연구센터) ;
  • 구성태 (부산대학교 한의학전문대학원 한의과학과)
  • Received : 2019.11.08
  • Accepted : 2019.12.18
  • Published : 2019.12.27

Abstract

Objectives : Microglia play a crucial role in electroacupuncture (EA) analgesia on neuropathic pain. The role of chemokines in producing analgesic effects of EA, however, is largely unknown. In the present study, we investigated the role of chemokines in producing analgesic effects of EA in the neuropathic pain model. Methods : Sprague-Dawley rats were randomly assigned into three groups (anesthetized group (ANE), non-acupoint EA group (NAP), and ST36 - GB34 EA group (ACU)). Neuropathic pain was induced by tight ligation of L5 spinal nerve. Mechanical and thermal hypersensitivity of hind paw was tested. Western blot tests and immunofluorescence assay for C-C motif chemokine ligand 2 (CCL2) levels and microglia activation were performed on spinal cord L5/6. EA was treated once daily from the 3rd day after surgery for 5 days. Results : EA treatments applied to ST36 and GB34 significantly reduced both mechanical and thermal hypersensitivity after two and three times of treatment, respectively. While CCL2 expression significantly increased in neuropathic rats, it was significantly reduced in the ACU. In addition, co-localization of CCL2 and activated microglia significantly decreased in the ACU compared to those of ANE and NAP in the spinal cord L5/L6 dorsal horn. Conclusions : The present results suggest that EA applied to ST36 and GB34 modulates the reduction of CCL2 release from the injured neurons and consequently decreases microglia activation in the spinal cord. Regulation of chemokine induced spinal activation of microglia plays a key role in analgesic effects of EA in the rat model of neuropathic pain.

Keywords

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