Repetitive pulsed magnetic stimulation attenuates neurogenic erectile dysfunction associated with the upregulation of the BDNF/NGF axis in a rat model of cavernous nerve injury

Iatrogenic cavernous nerve (CN) injury remains a prevalent complication following radical prostatectomy, leading to refractory erectile dysfunction (ED). While magnetic stimulation has shown neuroregenerative potential in other contexts, its therapeutic efficacy and molecular mechanisms in post-prostatectomy ED remain poorly defined. The aim of this study was to investigate whether repetitive pulsed magnetic stimulation (rPMS) facilitates neurovascular preservation and erectile function recovery in a rat model of bilateral CN crush injury. Thirty adult male Sprague Dawley rats were randomly assigned to three groups ( n = 10 per group): sham surgery (Sham group), bilateral CN crush alone (BCNC group), and BCNC followed by rPMS treatment (rPMS group). The BCNC model was established by bilateral compression of the CNs. Starting three days postoperatively, the rPMS group underwent a two-week regimen of 10 Hz stimulation (15% maximum output; 2400 pulses per session) every other day, totaling six sessions. Erectile function was evaluated via CN electrostimulation. Penile tissue and CN samples were subsequently harvested to assess nerve repair and corpus cavernosum histology. A functional assessment demonstrated that rPMS significantly restored the maximum intracavernosal pressure (Max ICP)/mean arterial pressure (MAP) ratio. At both the molecular level and the ultrastructural level, rPMS therapy reduced corporal fibrosis and apoptosis while promoting axonal repair. These structural improvements correlated with the upregulation of the brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) neurotrophic signaling pathways within the injured CN. rPMS significantly improved erectile hemodynamics in a rat model of CN injury. This functional recovery is closely associated with an enhanced neurotrophic microenvironment involving BDNF and NGF.