Abstract
Background: Neurogenic bladder (NB) is a type of neurological bladder dysfunction characterized by increased detrusor muscle contraction. Adenosine triphosphate (ATP)-P2X receptor signaling plays a role in muscle contraction. This study aimed to explore whether ATP-P2X signaling is involved in the mechanism through which electroacupuncture (EA) affects excessive detrusor muscle contraction in NB.
Methods: Forty rats were divided into CON, NB, SHAM, PPADS (a P2X1/2 receptor antagonist), and EA groups. The NB model was induced using the modified Hassan Shaker spinal cord transection method. After one week of EA treatment, urodynamic tests were used to assess bladder function, hematoxylin and eosin (H&E) staining was used to evaluate morphological changes, enzyme-linked immunosorbent assays (ELISAs) were used to measure ATP concentrations, and Western blotting was used to analyze the protein levels of P2X1, P2X2, phosphorylated myosin light chain kinase (p-MLCK), and phosphorylated myosin light chain (p-MLC).
Results: NB treatment led to morphological abnormalities, impaired urodynamics, increased ATP/P2X1/P2X2/p-MLC levels (P<0.01), and decreased p-MLCK protein levels (P<0.01). Both EA and the P2X1/2 receptor antagonist reversed these changes induced by NB dysfunction (P<0.05).
Conclusion: The findings suggest that the ATP-P2X signaling pathway is involved in the therapeutic effect of EA on excessive detrusor contraction in a rat model of NB.