IBRO neuroscience reports · 2025
Electroacupuncture enhances nerve regeneration and functional recovery in a rat model of median nerve transection.
СтатьяНазвание и аннотация: Перевод в очереди
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Zhou Hongyu, He Jin, Yalikun Ainizier, Chen Hui, Aierken Rehemulatu Yu Si, Li Li
Аннотация
OBJECTIVE: To investigate the therapeutic efficacy and underlying mechanisms of electroacupuncture (EA) in promoting peripheral nerve regeneration following delayed repair of a median nerve transection in a rat model.
METHODS: Thirty male Sprague-Dawley rats were randomly assigned to five groups: sham operation, model (1- and 2-weeks post-transection), and EA treatment (1- and 2-weeks post-repair). Median nerve transection was performed, followed by delayed microsurgical repair. EA was applied at Jianyu (LI15) and Neiguan (PC6) acupoints following nerve repair. Nerve regeneration and tissue response were evaluated through histological staining (Hematoxylin and Eosin [H&E], Luxol Fast Blue [LFB], Masson's Trichrome [Masson]), immunofluorescence (S100β, Sox10), western blotting (phosphorylated phosphoinositide 3-kinase [p-PI3K], receptor for advanced glycation end products [RAGE], triggering receptor expressed on myeloid cells 2 [TREM2]), enzyme-linked immunosorbent assay (ELISA; interleukin-6 [IL-6], C-X-C motif chemokine ligand 3 [CXCL3], matrix metalloproteinase-3 [MMP3], reactive oxygen species [ROS], superoxide dismutase [SOD], malondialdehyde [MDA]), and transcriptome sequencing with gene set enrichment analysis (GSEA).
RESULTS: EA significantly enhanced axonal regeneration and remyelination, reduced inflammatory infiltration, and suppressed fibrotic collagen deposition. EA treatment markedly downregulated p-PI3K and RAGE expression and upregulated TREM2, indicating inhibition of inflammatory signaling and promotion of M2 macrophage polarization. Serum biomarkers showed reduced levels of IL-6, ROS, and MDA, along with increased SOD activity. Transcriptomic analysis revealed EA-induced activation of reparative and metabolic pathways, including lysosome function, endocytosis, and protein processing, while reversing injury-induced suppression of oxidative phosphorylation and ribosomal function.
CONCLUSION: EA facilitates peripheral nerve regeneration through multi-target regulation of inflammation, oxidative stress, and neuroglial activity. These findings support the translational potential of EA as a complementary therapeutic strategy following nerve repair for upper limb peripheral nerve injuries.
METHODS: Thirty male Sprague-Dawley rats were randomly assigned to five groups: sham operation, model (1- and 2-weeks post-transection), and EA treatment (1- and 2-weeks post-repair). Median nerve transection was performed, followed by delayed microsurgical repair. EA was applied at Jianyu (LI15) and Neiguan (PC6) acupoints following nerve repair. Nerve regeneration and tissue response were evaluated through histological staining (Hematoxylin and Eosin [H&E], Luxol Fast Blue [LFB], Masson's Trichrome [Masson]), immunofluorescence (S100β, Sox10), western blotting (phosphorylated phosphoinositide 3-kinase [p-PI3K], receptor for advanced glycation end products [RAGE], triggering receptor expressed on myeloid cells 2 [TREM2]), enzyme-linked immunosorbent assay (ELISA; interleukin-6 [IL-6], C-X-C motif chemokine ligand 3 [CXCL3], matrix metalloproteinase-3 [MMP3], reactive oxygen species [ROS], superoxide dismutase [SOD], malondialdehyde [MDA]), and transcriptome sequencing with gene set enrichment analysis (GSEA).
RESULTS: EA significantly enhanced axonal regeneration and remyelination, reduced inflammatory infiltration, and suppressed fibrotic collagen deposition. EA treatment markedly downregulated p-PI3K and RAGE expression and upregulated TREM2, indicating inhibition of inflammatory signaling and promotion of M2 macrophage polarization. Serum biomarkers showed reduced levels of IL-6, ROS, and MDA, along with increased SOD activity. Transcriptomic analysis revealed EA-induced activation of reparative and metabolic pathways, including lysosome function, endocytosis, and protein processing, while reversing injury-induced suppression of oxidative phosphorylation and ribosomal function.
CONCLUSION: EA facilitates peripheral nerve regeneration through multi-target regulation of inflammation, oxidative stress, and neuroglial activity. These findings support the translational potential of EA as a complementary therapeutic strategy following nerve repair for upper limb peripheral nerve injuries.