Article(id=1286995091617190781, tenantId=1146029695717560320, journalId=1285991164901855263, issueId=1286995055894315111, articleNumber=null, orderNo=null, doi=10.3969/j.issn.1001-1242.2026.07.002, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1714924800000, receivedDateStr=2024-05-06, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1784773141053, onlineDateStr=2026-07-23, pubDate=1784044800000, pubDateStr=2026-07-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1784773141053, onlineIssueDateStr=2026-07-23, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1784773141053, creator=13701087609, updateTime=1784773141053, updator=13701087609, issue=Issue{id=1286995055894315111, tenantId=1146029695717560320, journalId=1285991164901855263, year='2026', volume='41', issue='7', pageStart='1009', pageEnd='1183', issueExtLink='null', onlineDate='null', pubDate='1784044800000', pubDateStr='2026-07-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1784773132536, creator='13701087609', updateTime=1784773687037, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1286997381702979733, tenantId=1146029695717560320, journalId=1285991164901855263, issueId=1286995055894315111, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1286997381702979734, tenantId=1146029695717560320, journalId=1285991164901855263, issueId=1286995055894315111, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1019, endPage=1027, ext={EN=ArticleExt(id=1286995091810128766, articleId=1286995091617190781, tenantId=1146029695717560320, journalId=1285991164901855263, language=EN, title=Effects of acupuncture on the AMPK/SIRT1/PGC-1α signaling pathway in skeletal muscle of aging rats, columnId=null, journalTitle=Chinese Journal of Rehabilitation Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=
Objective: To observe the effect of acupuncture on the AMPK/SIRT1/PGC- 1α signaling pathway in skeletal muscle of aging rats, and to explore the possible mechanism of acupuncture in delaying aging skeletal muscle atrophy in lumbar skeletal muscle.
Method: Forty male SD rats were randomly divided into blank group, model group, acupuncture group and non-acupoint group. The blank group received daily subcutaneous injections of normal saline in the dorsal neck region. The other three groups received daily subcutaneous injections of D-galactose (D-gal) in the same region for 12 weeks to induce aging. Starting from week 9, acupuncture intervention was performed for 4 weeks. The acupuncture group took bilateral L3—L5 Jiaji points, and the non-acupoint group took bilateral non-meridian and non-acupoint points. Body weight and growth rates were measured, and muscle strength was evaluated using a grip strength test. Lumbar skeletal muscle atrophy was assessed using hematoxylin and eosin staining. Serum levels of superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-PX) were analyzed biochemically. Relative expression levels of AMPKα, SIRT1, PGC-1α, P21 and P53 mRNA were detected by real-time quantitative PCR.
Result: Compared with the blank group, the body weight of the model group, the acupuncture group and the non-acupoint group was reduced (P<0.01, P<0.05, P<0.01), and the difference in terminal body weight growth rate was significant (P<0.001 for all). Before intervention, grip strength was significantly reduced in all experimental groups compared to the blank group (P<0.01 for all), with no significant differences among the experimental groups (P>0.05). After the intervention, the model group showed significantly lower grip strength compared to the blank group (P<0.001), accompanied by evident lumbar skeletal muscle atrophy, as reflected by reduced muscle fiber area and diameter (P<0.001, P<0.01). Additionally, serum SOD and GSH-PX activities decreased (P<0.001, P<0.001), while MDA increased significantly (P<0.01). The mRNA expression levels of AMPKα, SIRT1, and PGC-1α decreased significantly (P<0.001, P<0.001, P<0.01), while the relative mRNA expression levels of P21 and P53 were higher than those in the blank group (P<0.05, P<0.01). Compared with the model group, the acupuncture group demonstrated increased grip strength (P<0.001), improved skeletal muscle fiber area and diameter (P<0.01, P<0.05), enhanced serum SOD and GSH-PX activities (P<0.001, P<0.01), reduced serum MDA levels (P<0.05), and elevated AMPKα, SIRT1, and PGC-1α mRNA expression (P<0.001, P<0.01, P<0.05). Moreover, P21 and P53 mRNA expression levels were significantly reduced in the acupuncture group (P<0.05, P<0.01), while there was no significant difference in the non-acupoint group (P>0.05).
Conclusion: Acupuncture at Jiaji points alleviated the atrophy of lumbar skeletal muscles, improved muscle strength and inhibited oxidative stress in aging rats. These effects may be mediated through the AMPK/SIRT1/PGC-1α signaling pathway.
, authors=Zhengyu YANG
1, Qun CHEN
2, Jing JIN
1, authorsList=Zhengyu YANG, Qun CHEN, Jing JIN, authorCompany=null, correspAuthors=null, 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=1286995092040815487, articleId=1286995091617190781, tenantId=1146029695717560320, journalId=1285991164901855263, language=CN, title=针刺夹脊穴对衰老模型大鼠骨骼肌AMPK/SIRT1/PGC-1α信号通路的影响, columnId=1286995083228582705, journalTitle=中国康复医学杂志, columnName=基础研究, runingTitle=null, highlight=null, articleAbstract=
目的： 观察针刺夹脊穴对衰老大鼠骨骼肌AMPK/SIRT1/PGC-1α信号通路的影响，探讨针刺延缓腰部骨骼肌衰老性骨骼肌萎缩的可能机制。
方法： 40只SD雄性大鼠随机分为空白组、模型组、针刺组、非穴组。空白组大鼠每日项背部皮下注射生理盐水，其余3组大鼠每日项背部皮下注射D-gal，每日1次，连续12周，自第9周起进行针刺干预。针刺组取双侧L3—L5夹脊穴，非穴组取大鼠双侧非经非穴，每日1次，持续4周。测量各组大鼠体重及终末体质量增长率，采用抓力测试检测大鼠肌力，HE染色观察大鼠腰部骨骼肌萎缩情况，生化检测大鼠血清超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-PX）含量，实时荧光定量PCR检测单磷酸腺苷活化蛋白激酶α（AMPKα）、沉默信息调节因子1（SIRT1）、过氧化物酶增殖物激活受体γ共激活因子1α（PGC-1α）、细胞周期蛋白依赖性激酶抑制因子1A（P21）、肿瘤抑制蛋白53（P53）mRNA的相对表达量。
结果： 同空白组相比，模型组、针刺组、非穴组大鼠体质量减轻（P<0.01，P<0.05，P<0.01），终末体重增长率差异有显著性（P<0.001，P<0.001，P<0.001）。干预前，与空白组相比，模型组、针刺组、非穴组大鼠抓力均下降（P<0.01，P<0.01，P<0.01），而3组大鼠之间的抓力无差异（P>0.05）。干预后，模型组大鼠抓力明显低于空白组（P<0.001），腰部骨骼肌细胞出现萎缩，具体表现在骨骼肌肌纤维面积和纤维直径下降（P<0.001，P<0.01），大鼠血清中SOD、GSH-PX的活力下降（P<0.001，P<0.001），MDA含量显著升高（P<0.01），腰部骨骼肌组织中AMPKα、SIRT1、PGC-1α mRNA表达显著降低（P<0.001，P<0.001，P<0.01），P21、P53 mRNA相对表达量比空白组高（P<0.05，P<0.01）。与模型组相比，针刺组大鼠抓力升高（P<0.001），大鼠腰部骨骼肌萎缩程度较模型组大鼠有所改善，骨骼肌肌纤维面积和直径增加（P<0.01，P<0.05），针刺夹脊穴上调了大鼠血清中SOD活力、GSH-PX活力（P<0.001，P<0.01），抑制了血清中MDA的表达（P<0.05），AMPKα、SIRT1、PGC-1α mRNA的表达量升高（P<0.001，P<0.01，P<0.05），P21、P53 mRNA相对表达量下降（P<0.05，P<0.01），而非穴组大鼠未见显著差异（P>0.05）。
结论： 针刺夹脊穴可使衰老模型大鼠腰部骨骼肌萎缩情况有所缓解，提高了衰老大鼠肌力，抑制氧化应激反应，这可能是通过AMPK/SIRT1/PGC-1α通路发挥作用。
, authors=杨正瑜
1, 陈群
2, 金京
1, 陈柏瑞
1, 王宇
1, 朱浩铭
1, 刘海潮
1, 林建平
3, 陈少清
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