Intervention of Bazi Bushen Capsule on Benign Prostatic Hyperplasia Concomitant with Erectile Dysfunction Induced by Testosterone Supplementation in Spontaneously Hypertensive Rats.

Objective: To explore the intrinsic relationship between benign prostatic hyperplasia (BPH) and erectile dysfunction (ED) and evaluate the therapeutic effects of Bazi Bushen Capsule (BZBS).

Methods: A model of BPH concomitant with ED was established by using testosterone-supplemented spontaneously hypertensive rats (SHRs). Forty SHRs were divided into 4 groups based on the random number table (n=10 per group), including the model group (SHR+T), the BZBS low-dose group (SHR+T+BZ-low), the BZBS high-dose group (SHR+T+BZ-high), and the finasteride group (SHR+T+Fi). Ten Wistar-Kyoto rats were set up as the control group. Except for the control group, SHRs were subcutaneously injected with 3 mg/kg testosterone, and treated with different therapeutic modalities at the same time for 28 days. The androgen signaling markers related to the prostate, markers of cell proliferation and apoptosis, indicators of corpus cavernosum fibrosis and contraction/relaxation function, inflammatory markers in the prostate and corpus cavernosum tissue were assessed. Network pharmacology analysis was conducted to identify the key therapeutic targets of BZBS and to further validate the experimental findings.

Results: BZBS significantly reduced prostate wet weight and prostate index, and improved pathological changes (P<0.01). BZBS modulated expressions of proliferating cell nuclear antigen, Bcl-2-associated X protein, and B-cell lymphoma 2 expression (P<0.05 or P<0.01). BZBS alleviated corpus cavernosum fibrosis, increased the smooth muscle area, upregulated α-smooth muscle actin expression, and improved functional markers-including Ras homolog family member A, Rho-associated coiled-coil containing protein kinase 2, endothelial nitric oxide synthase, nitric oxide, and cyclic guanosine monophosphate (P<0.05 or P<0.01). BZBS also regulated androgen levels, including dihydrotestosterone, 5α-reductase type II, and prostate-specific antigen (P<0.05 or P<0.01). Notably, BZBS effectively attenuated inflammatory responses in both the prostate and corpus cavernosum tissue (P<0.05 or P<0.01). Unlike finasteride-which primarily reduces prostate inflammation-BZBS exhibited a dual therapeutic effect on both BPH and ED. Network pharmacology further suggested that BZBS exerts its effects through multiple inflammation-related targets and pathways.

Conclusions: Chronic inflammation plays a crucial role in both BPH and ED. BZBS effectively ameliorates these conditions by modulating inflammatory processes.