Electroacupuncture Alleviates Neuropathic Pain through Regulating miR-206-3p Targeting BDNF after CCI.

IF 3 4区医学 Q2 NEUROSCIENCES

Neural Plasticity Pub Date : 2022-06-09 eCollection Date: 2022-01-01 DOI:10.1155/2022/1489841

Wenzhan Tu, Jingjing Yue, Xuqing Li, Qiaoyun Wu, Guanhu Yang, Shengcun Li, Qiangsan Sun, Songhe Jiang

{"title":"Electroacupuncture Alleviates Neuropathic Pain through Regulating miR-206-3p Targeting BDNF after CCI.","authors":"Wenzhan Tu, Jingjing Yue, Xuqing Li, Qiaoyun Wu, Guanhu Yang, Shengcun Li, Qiangsan Sun, Songhe Jiang","doi":"10.1155/2022/1489841","DOIUrl":null,"url":null,"abstract":"Background: Electroacupuncture (EA) has benefits for neuropathic pain. However, the underlying mechanisms are still unknown. The current study explores the underlying mechanisms of EA in neuropathic pain of chronic constriction injury (CCI) rats. Material/Methods. Overall, 126 Sprague-Dawley (200-250 g) rats were divided into nine groups randomly: the sham-operated, CCI, CCI+EA, CCI+sham EA, CCI+NS, CCI+AAV-NC, CCI+AAV-miR-206-3p, CCI+EA+NS, and CCI+EA+AAV-miR-206-3p groups. The animals were sacrificed 14 days postsurgery. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) tests were used to determine differences in neurobehavioral manifestations. qPCR, western blotting, and immunofluorescence (IF) were carried out to detect the expression levels of miR-206-3p, BDNF, BAX/Bcl-2, TNF-α, and IL-6. Nissl staining was measured to observe morphological changes in neurons. Transmission electron microscopy (TEM) was employed to evaluate microscopic changes in dorsal horn synapses.Results: Hyperalgesia was reduced markedly by EA in the CCI model. The expression level of miR-206-3p was elevated, whereas the expression levels of BDNF, BAX/Bcl-2, TNF-α, and IL-6 were decreased in EA-treated CCI rats. However, a miR-206-3p inhibitor partially abrogated the analgesic effect of EA and resulted in poor behavioral performance and the BDNF, BAX/Bcl-2, TNF-α, and IL-6 expression was elevated as well.Conclusions: EA can relieve neuropathic pain by regulating the miR-206-3p/BDNF pathway, thus exerting anti-inflammatory and antiapoptotic effect.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":null,"pages":null},"PeriodicalIF":3.0000,"publicationDate":"2022-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9203241/pdf/","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neural Plasticity","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1155/2022/1489841","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}

引用次数: 3

Abstract

Background: Electroacupuncture (EA) has benefits for neuropathic pain. However, the underlying mechanisms are still unknown. The current study explores the underlying mechanisms of EA in neuropathic pain of chronic constriction injury (CCI) rats. Material/Methods. Overall, 126 Sprague-Dawley (200-250 g) rats were divided into nine groups randomly: the sham-operated, CCI, CCI+EA, CCI+sham EA, CCI+NS, CCI+AAV-NC, CCI+AAV-miR-206-3p, CCI+EA+NS, and CCI+EA+AAV-miR-206-3p groups. The animals were sacrificed 14 days postsurgery. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) tests were used to determine differences in neurobehavioral manifestations. qPCR, western blotting, and immunofluorescence (IF) were carried out to detect the expression levels of miR-206-3p, BDNF, BAX/Bcl-2, TNF-α, and IL-6. Nissl staining was measured to observe morphological changes in neurons. Transmission electron microscopy (TEM) was employed to evaluate microscopic changes in dorsal horn synapses.

Results: Hyperalgesia was reduced markedly by EA in the CCI model. The expression level of miR-206-3p was elevated, whereas the expression levels of BDNF, BAX/Bcl-2, TNF-α, and IL-6 were decreased in EA-treated CCI rats. However, a miR-206-3p inhibitor partially abrogated the analgesic effect of EA and resulted in poor behavioral performance and the BDNF, BAX/Bcl-2, TNF-α, and IL-6 expression was elevated as well.

Conclusions: EA can relieve neuropathic pain by regulating the miR-206-3p/BDNF pathway, thus exerting anti-inflammatory and antiapoptotic effect.

Abstract Image

查看原文本刊更多论文

电针通过调节靶向BDNF的miR-206-3p缓解CCI后神经性疼痛。

背景:电针(EA)对神经性疼痛有疗效。然而，其潜在机制尚不清楚。本研究旨在探讨EA在慢性收缩性损伤(CCI)大鼠神经性疼痛中的作用机制。材料/方法。将126只Sprague-Dawley (200-250 g)大鼠随机分为9组:假手术组、CCI组、CCI+EA组、CCI+sham EA组、CCI+NS组、CCI+AAV-NC组、CCI+AAV-miR-206-3p组、CCI+EA+NS组和CCI+EA+AAV-miR-206-3p组。术后14天处死动物。使用机械戒断阈值(MWT)和热戒断潜伏期(TWL)测试来确定神经行为表现的差异。采用qPCR、western blotting和免疫荧光(IF)检测miR-206-3p、BDNF、BAX/Bcl-2、TNF-α、IL-6的表达水平。采用尼氏染色法观察神经元形态学变化。透射电镜(TEM)观察背角突触的显微变化。结果:EA能明显减轻CCI模型的痛觉过敏。ea处理的CCI大鼠miR-206-3p表达水平升高，BDNF、BAX/Bcl-2、TNF-α、IL-6表达水平降低。然而，miR-206-3p抑制剂部分取消了EA的镇痛作用，导致行为表现不佳，BDNF、BAX/Bcl-2、TNF-α和IL-6的表达也升高。结论:EA可通过调节miR-206-3p/BDNF通路减轻神经性疼痛，发挥抗炎、抗凋亡作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Neural Plasticity NEUROSCIENCES-

CiteScore

6.80

自引率

0.00%

发文量

审稿时长

16 weeks

期刊介绍： Neural Plasticity is an international, interdisciplinary journal dedicated to the publication of articles related to all aspects of neural plasticity, with special emphasis on its functional significance as reflected in behavior and in psychopathology. Neural Plasticity publishes research and review articles from the entire range of relevant disciplines, including basic neuroscience, behavioral neuroscience, cognitive neuroscience, biological psychology, and biological psychiatry.