Article(id=1291404922726113950, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404875351449891, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.09.015, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1733673600000, receivedDateStr=2024-12-09, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824526720, onlineDateStr=2026-08-04, pubDate=1747411200000, pubDateStr=2025-05-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824526720, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824526720, creator=13701087609, updateTime=1785824526720, updator=13701087609, issue=Issue{id=1291404875351449891, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='9', pageStart='1201', pageEnd='1350', issueExtLink='null', onlineDate='null', pubDate='1747411200000', pubDateStr='2025-05-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824515426, creator='13701087609', updateTime=1785824515426, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=1286, endPage=1291, ext={EN=ArticleExt(id=1291404922956800671, articleId=1291404922726113950, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Effects of lidocaine on pain threshold in rats with myofascial pain syndrome by activating cAMP/PKA/PGC-1α signaling pathways, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the effects of 1% lidocaine on pain threshold in rats with myofascial pain syndrome (MPS) based on cyclic adenosine monophosphate (cAMP) / protein kinase A (PKA)/peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) signaling pathways.
Methods The models of MPS rats were prepared by striking manipulation + fatigue method, and they were randomly divided into model group, combined group, experimental-L group and experimental-H group, 10 rats in each group. Another 10 rats were selected as blank group. After successful molding, experimental-L group and experimental-H group were given injection of 1% lidocaine (0.25 mL, 0.5 mL) at pain trigger site of right medial thigh (once a week), combined group was given intraperitoneal injection of SR-18292 (30 mg·kg-1, 3 times a week) on basis of experimental-H group, model group and blank group were given injection of normal saline (once a week) at pain trigger site of right medial thigh or at the same site. Five groups were treated for 3 weeks. The pain threshold was detected by mechanical stimulation and thermal stimulation, level of adenosine triphosphate (ATP) in muscle tissues at pain trigger site was detected by the kit, and expressions of cAMP, PKA and PGC-1α proteins were detected by Western blot.
Results After 3 weeks of intervention, paw withdrawal mechanical threshold (PWMT) values in experimental-H group, combined group, model group and blank group were (51.69±7.22), (37.84±6.29), (20.33±5.83) and (67.88±8.46) g, paw withdrawal latency (PWL) values were (10.58±1.03), (7.89±0.87), (6.33±0.92) and (12.89±1.64) s, ATP levels were (866.37±98.66), (728.81±89.60), (617.52±89.84) and (1 098.45±101.36) μmol·g-1, relative expression levels of cAMP protein were 0.53±0.08, 0.48±0.07, 0.21±0.06 and 0.68±0.10, relative expression levels of PKA protein were 0.60±0.06, 0.58±0.08, 0.28±0.05 and 0.79±0.09, relative expression levels of PGC-1α protein were 0.78±0.05, 0.59±0.06, 0.41±0.08 and 0.93±0.09, and the differences were statistically significant between experimental-H group, combined group and mode group (all P<0.05).
Conclusion 1% lidocaine can improve pain threshold and mitochondrial energy metabolism in muscle tissues of affected limbs in MPS rats, which may be related to activating cAMP/PKA/PGC-1α signaling pathways.
, authors=Hong TAO, Xi-ming LIU, Chun-kui WANG, authorsList=Hong TAO, Xi-ming LIU, Chun-kui WANG, authorCompany=null, correspAuthors=Chun-kui WANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291404923359453856, articleId=1291404922726113950, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=利多卡因激活cAMP/PKA/PGC-1α信号通路对肌筋膜疼痛综合征大鼠痛阈的影响, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 基于环腺苷酸（cAMP）/蛋白激酶A（PKA）/过氧化物酶体增殖物激活受体γ共激活因子-1α（PGC-1α）信号通路探讨1%利多卡因对肌筋膜疼痛综合征（MPS）大鼠痛阈的影响。
方法 用击打法联合疲劳法制备MPS大鼠模型，并随机分为模型组、联合组和低、高剂量实验组，每组10只；另选取10只正常大鼠作为空白组。造模成功后，低、高剂量实验组于右股内侧的疼痛触发点处注射1%利多卡因0.25、0.50 mL，每周1次；联合组于右股内侧的疼痛触发点处注射1%利多卡因0.50 mL，每周1次+腹腔注射30 mg·kg-1 SR-18292，每周3次；模型组和空白组均于右股内侧疼痛触发点或相同位置注射0.9% NaCl，每周1次。5组大鼠均连续给药3周。用机械刺激和热刺激法检测疼痛阈值，用试剂盒测定疼痛触发点肌肉组织中腺苷三磷酸（ATP）的水平，用蛋白质印迹法检测cAMP、PKA和PGC-1α蛋白的表达水平。
结果 干预3周后，高剂量实验组、联合组、模型组和空白组的机械刺激缩足阈值（PWMT）分别为（51.69±7.22）、（37.84±6.29）、（20.33±5.83）和（67.88±8.46）g，缩足潜伏期（PWL）分别为（10.58±1.03）、（7.89±0.87）、（6.33±0.92）和（12.89±1.64）s，ATP水平分别为（866.37±98.66）、（728.81±89.60）、（617.52±89.84）和（1 098.45±101.36）μmol·g-1，cAMP蛋白相对表达水平分别为0.53±0.08、0.48±0.07、0.21±0.06和0.68±0.10，PKA蛋白相对表达水平分别为0.60±0.06、0.58±0.08、0.28±0.05和0.79±0.09，PGC-1α蛋白相对表达水平分别为0.78±0.05、0.59±0.06、0.41±0.08和0.93±0.09；高剂量实验组和联合组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 1%利多卡因能提高MPS大鼠的疼痛阈值，改善患肢肌肉组织线粒体能量代谢，可能与激活cAMP/PKA/PGC-1α信号通路有关。
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陶宏（1977-），男，副主任医师，主要从事临床麻醉、疼痛治疗的相关研究
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