Electroacupuncture ameliorates bladder dysfunction and fibrosis in diabetic rats: Underlying role of transient receptor potential vanilloid 1 in the dorsal root ganglion

Objective: To assess the therapeutic effects of electroacupuncture (EA) in a rat model of diabetic cystopathy (DCP) and examine its impact on the expression of transient receptor potential vanilloid 1 (TRPV1) in the dorsal root ganglion (DRG). Methods: Sixty male Sprague-Dawley rats were divided into four groups: control, DCP, EA, and sham EA (n = 10). DCP was induced using a high-fat diet, followed by streptozotocin injection. EA was administered at the Pangguangshu (BL 28) and Sanyinjiao (SP 6) acupoints for 8 weeks. Bladder function, structure, and molecular changes were evaluated using ultrasonography, urodynamic tests, bladder weight measurements, histological stainings (hematoxylin and eosin and Masson's trichrome stainings), transmission electron microscopy, immunohistochemical analysis, and Western blot for TRPV1 expression in the DRG. Results: The DCP group exhibited significantly increased bladder weight, wall thickness, collagen fiber expression, maximum bladder capacity (MBC), post-void residual (PVR), and leakage point pressure, along with reduced bladder compliance (BC) and voiding efficiency (V%) compared with the control group (all P < .05). EA treatment significantly decreased bladder weight (P = .003), collagen deposition (P = .002), wall thickness (P = .027), MBC (P = .046), and PVR (P = .023), and increased BC (P = .048) and V% (P = .022) compared with sham EA. Ultrastructural damage in DRG neurons was markedly ameliorated by EA. TRPV1 protein expression in the DRG was significantly higher in the EA group than in the sham EA group (immunohistochemistry: P = .003; Western blot: P = .001). Conclusion: EA alleviates bladder dysfunction and remodeling in DCP rats, an effect associated with upregulated TRPV1 expression in the DRG, reduced bladder fibrosis, and preserved neuronal ultrastructure. These findings suggest a potential role for TRPV1 signaling in mediating the therapeutic effects of EA, warranting further functional investigation.