Potential repositioning of GV1001 as a therapeutic agent for testosterone‑induced benign prostatic hyperplasia

Abstract

Benign prostatic hyperplasia (BPH) is one of the leading causes of male reproductive disorders. Therapeutic agents currently in use have severe side effects; therefore, alternative drugs that exhibit improved therapeutic activity without side effects are required. The present study investigated the protective effect of GV1001 against testosterone‑induced BPH in rats. BPH in castrated rats was established via daily subcutaneous (s.c.) injections of testosterone propionate (TP, 3 mg/kg) dissolved in corn oil for 4 weeks. GV1001 (0.01, 0.1 and 1 mg/kg, s.c.) was administered 3 times per week for 4 weeks, together with TP (3 mg/kg) injection. The rats were sacrificed on the last day of treatment, and their prostates were excised and weighed for biochemical and histological studies. Serum levels of testosterone and dihydrotestosterone (DHT) were also measured. In rats with TP‑induced BPH, a significant increase in prostate weight (PW) and prostatic index (PI), accompanied by a decrease in antioxidant enzyme activity, was observed. Histological studies revealed clearly enlarged glandular cavities in rats with BPH. GV1001 (0.01 and 0.1 mg/kg) treatment significantly decreased PW and PI in rats with TP‑induced BPH. In addition, GV1001 demonstrated a potent inhibitory effect on 5α‑reductase in prostate. The present data suggest that the protective role of GV1001 against testosterone‑induced BPH is closely associated with its antioxidant potential. Additional studies are required to identify the mechanisms by which GV1001 protects against BPH to determine its clinical application.

GV1001 inhibits cell viability and induces apoptosis in castration-resistant prostate cancer cells through the AKT/NF-κB/VEGF pathway

“…In addition to our data demonstrating effects on the AKT/NF-κB/VEGF pathway, GV1001 exhibits several potential biological mechanisms of action, with involvement in the TGF-β signaling pathway 25, the hypoxia-induced HIF-1α-VEGF signaling axis 19, and the ERK and p38 MAP kinase pathway 26. In addition, GV1001 inhibits gonadotropin-releasing hormone (GnRH) and 5α‑reductase, which are important in prostate cancer 27, 28. Kim et al reported that GV1001 can be a therapeutic agent for testosterone-induced benign prostatic hyperplasia (BPH) 27.…”

“…In addition, GV1001 inhibits gonadotropin-releasing hormone (GnRH) and 5α‑reductase, which are important in prostate cancer 27, 28. Kim et al reported that GV1001 can be a therapeutic agent for testosterone-induced benign prostatic hyperplasia (BPH) 27. After establishing BPH in castrated rats via daily subcutaneous injections of testosterone propionate, GV1001 was administered for 4 weeks.…”

Ellagic acid improves benign prostate hyperplasia by regulating androgen signaling and STAT3

“…Increased expressions of AR, 5AR2, and PSA correlate with prostate hyperplasia, and these markers are increased markedly in patients and in animal models with BPH [ 21 , 22 ]. The experimental BPH animal models induced by chronic injection of TP have been widely used to confirm etiological and pathophysiological evidence as well as pharmacological evidence for BPH [ 23 , 24 ]. The present study used the TP-induced BPH rat model to investigate the therapeutic effect of EA and we found that EA significantly reduced the prostate size, epithelial thickness, serum DHT levels, and the protein levels of AR, 5AR2, and PSA in the TP-induced BPH rat model.…”

Testosterone improves muscle function of the extensor digitorum longus in rats with sepsis

“…Furthermore, testosterone propionate has androgen-like effects. Long-term usage of exogenous androgen may inhibit male gonads, and common complications include testicular atrophy and prostatic hyperplasia, which severely limits its clinical application [20]. Therefore, medicinal plants have been exploited to screen new agents with androgen-like effects [21,22].…”