Modulatory mechanisms of electroacupuncture in fascial tissue repair: a pilot study using a rat model of thoracolumbar fasciitis

医学 电针 大鼠模型 针灸科 筋膜炎 外科 麻醉 成纤维细胞 足底筋膜炎 筋膜 慢性疼痛 疼痛管理 术后疼痛 治疗效果 结节性筋膜炎 脉动式射频电磁波 病理
作者
Xiubing Tong,Debiao Yu,Jiayan Chen,Linyao Zheng,Yanping Fang,Jingyu Zhang,Tianyu Rao,Kezhi Liu,Jia Lin,Yu KAN,Yuye Lin,Chufan Zeng,Guojun Zhang,X. Q. Zhang,Xianghong Jing,Yuting Huang,Jun Liao
出处
期刊:Acupuncture in Medicine [SAGE Publishing]
卷期号:44 (1): 49-61
标识
DOI:10.1177/09645284251410580
摘要

Introduction: Myofasciitis, a prevalent cause of musculoskeletal pain, is associated with thoracolumbar fascial changes. Acupuncture is effective for pain relief, but its role in fascial repair remains unclear. This study examined the effects of electroacupuncture (EA) at BL23 ( Shenshu ) and BL40 ( Weizhong ) on fascial tissue repair in a rat model of thoracolumbar fasciitis (TLF). Methods: The study involved 42 six-week-old Sprague–Dawley rats divided into control ( n = 15) and modeling ( n = 27) groups. TLF was induced by injecting complete Freund’s adjuvant into the thoracolumbar fascia. Three rats in the control and modeling groups were used for model validation. The remaining 24 modeled rats were split into model and EA groups ( n = 12 each). EA was administered at BL23 and BL40 to rats in the EA group for 20 min daily for 9 days. Assessments included skin pain sensitivity, musculoskeletal ultrasound, histological evaluation of fascial thickness, and measurement of inflammatory markers and fibroblast activity. Results: EA-treated rats showed significant improvements, including reduced mechanical pain sensitivity, decreased fascial thickness and lower expression of pro-inflammatory markers (tumor necrosis factor-α, interleukin 1β) and fibroblast activity markers (proliferating cell nuclear antigen, α-smooth muscle actin, and vimentin). There was also a favorable balance in extracellular matrix components (increased type I/III collagen and matrix metalloproteinase (MMP)-1/tissue inhibitor of MMP (TIMP)-1 ratios), which was linked to reduced activity of the transforming growth factor (TGF)-β1/suppressor of mother against decapentaplegic (Smad)2 pathway. Conclusion: EA at BL23 and BL40 reduces inflammation, inhibits fibroblast proliferation and activation, and promotes fascial repair, likely via modulation of the TGF-β1/Smad2 pathway. These findings support the therapeutic potential of EA for the treatment of myofasciitis, potentially aiding in chronic musculoskeletal pain management and fascial tissue repair.
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