| Objective To investigate the effects of Warm acupuncture on postmenopausal osteoporosis (PMOP) through individual or combined stimulation of lumbar-dorsal spinal acupoints and lesion points of tendon nodes. Methods Thirty C57BL/6 mice were randomly divided into five groups (n=6 per group): sham-operated group, model group, warm acupuncture I group, warm acupuncture II group, and warm acupuncture III group. PMOP models were established via bilateral ovariectomy and treated with warm acupuncture for 4 weeks. Femoral bone mineral density (BMD) was analyzed using micro-CT. Pathological changes and collagen fiber regeneration in femoral tissues were observed via hematoxylin-eosin (HE) and Masson staining. Serum concentrations of estradiol (E2), osteocalcin (BGP), type I collagen cross-linked C-terminal telopeptide (ICTP), tartrate-resistant acid phosphatase (TRACP), and bone alkaline phosphatase (BALP) were measured by ELISA. Protein expression levels of PI3K, AKT, and mTOR in femoral tissues were detected via Western blot. Results Compared with the sham-operated group, the model group exhibited decreased BMD, trabecular bone volume, and serum E2 and BGP levels (P < 0.05), while ICTP, TRACP, and BALP levels were increased (P < 0.05). Warm acupuncture treatment increased BMD, trabecular bone volume, and collagen fiber density. Among the three warm acupuncture groups, warm acupuncture III demonstrated the strongest regulatory effects on E2, ICTP, and BGP (P < 0.05). Western blot results showed that PI3K, AKT, and mTOR protein expression levels in the model group were lower than those in the sham-operated group (P < 0.001), whereas warm acupuncture-treated groups exhibited higher expression levels than the model group (P < 0.01), with warm acupuncture III showing the most pronounced upregulation (P < 0.01). Conclusion Combined stimulation of lumbar-dorsal spinal acupoints and lesion points of tendon nodes through warm acupuncture promotes BMD elevation, trabecular bone and collagen fiber regeneration, and bone metabolism regulation, thereby ameliorating PMOP. The underlying mechanism involves activation of the PI3K/AKT/mTOR signaling pathway. |