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浮针疗法通过调节慢性周围神经痛大鼠的线粒体稳态促进肌肉修复。

Fu's subcutaneous needling facilitates muscle repair by regulating mitochondrial homeostasis in rat with chronic peripheral nervous pain.

作者信息

Chiu Po-En, Fu Zhonghua, Pan Hung-Chuan, Tsai Yi-Ching, Tsai Chia-Yun, Hsu Wei-Jen, Chou Li-Wei, Lai De-Wei

机构信息

Department of Chinese Medicine, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan.

Graduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan.

出版信息

Front Physiol. 2025 Aug 21;16:1640735. doi: 10.3389/fphys.2025.1640735. eCollection 2025.

DOI:10.3389/fphys.2025.1640735
PMID:40917807
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12408641/
Abstract

Sciatica, often resulting from lumbar disc herniation or nerve compression, disrupts electrical signal transmission, leading to muscle atrophy, mitochondrial dysfunction, and impaired energy metabolism. This study explored the therapeutic effects of Fu's subcutaneous needling (FSN) in a chronic constriction injury (CCI) rat model, assessing its impact on neuropathic pain, muscle mass, and structural integrity. Histological and ultrastructural analyses demonstrated that FSN alleviated hypersensitivity, reduced muscle atrophy, preserved mitochondrial density, and maintained glycogen storage. Gene expression and pathway enrichment analyses revealed FSN's involvement in PI3K-Akt, MAPK signaling, oxidative phosphorylation, and mitophagy, suggesting its role in modulating energy metabolism and cellular repair. FSN also normalized energy-related proteins FGFR1, FGFR3 and phosphorylated FOXO3, highlighting their significance in muscle repair and regeneration. These findings provide novel insights into FSN's potential for counteracting neuropathy-induced muscle damage and improving mitochondrial function, supporting its clinical application. Additionally, FSN's role in muscle repair suggests a connection between growth factor signaling and nerve regeneration, offering a foundation for future research on muscle-neural recovery mechanisms.

摘要

坐骨神经痛通常由腰椎间盘突出或神经受压引起,会扰乱电信号传递,导致肌肉萎缩、线粒体功能障碍和能量代谢受损。本研究在慢性压迫性损伤(CCI)大鼠模型中探究了浮针疗法(FSN)的治疗效果,评估其对神经性疼痛、肌肉质量和结构完整性的影响。组织学和超微结构分析表明,浮针疗法减轻了超敏反应,减少了肌肉萎缩,保留了线粒体密度,并维持了糖原储存。基因表达和通路富集分析显示,浮针疗法参与了PI3K-Akt、MAPK信号传导、氧化磷酸化和线粒体自噬,表明其在调节能量代谢和细胞修复中的作用。浮针疗法还使能量相关蛋白FGFR1、FGFR3和磷酸化FOXO3正常化,突出了它们在肌肉修复和再生中的重要性。这些发现为浮针疗法对抗神经病变引起的肌肉损伤和改善线粒体功能的潜力提供了新见解,支持其临床应用。此外,浮针疗法在肌肉修复中的作用表明生长因子信号传导与神经再生之间存在联系,为未来关于肌肉-神经恢复机制的研究奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/a6471d160bee/fphys-16-1640735-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/ceb0fc29cd90/fphys-16-1640735-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/a05b5b16e56d/fphys-16-1640735-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/7f82865a495d/fphys-16-1640735-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/2e3ec9a75b94/fphys-16-1640735-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/8802cde1ffa2/fphys-16-1640735-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/2adaf244a160/fphys-16-1640735-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/f9b623bf3438/fphys-16-1640735-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/b0f8a8c39622/fphys-16-1640735-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/a6471d160bee/fphys-16-1640735-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/ceb0fc29cd90/fphys-16-1640735-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/a05b5b16e56d/fphys-16-1640735-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/7f82865a495d/fphys-16-1640735-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/2e3ec9a75b94/fphys-16-1640735-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/8802cde1ffa2/fphys-16-1640735-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/2adaf244a160/fphys-16-1640735-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/f9b623bf3438/fphys-16-1640735-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/b0f8a8c39622/fphys-16-1640735-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1909/12408641/a6471d160bee/fphys-16-1640735-g009.jpg

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