Effect of silodosin, an alpha1a-adrenoceptor antagonist, on benign prostatic hyperplasia in rat

Abstract

Objective To investigate the effect of silodosin, a selective alpha1a- adrenoceptor antagonist on a rat model of testosterone-induced benign prostatic hyperplasia (BPH) and its mechanisms. Methods The rats were divided into three groups: control, testosterone-induced BPH, and silodosin+ BPH groups. BPH was induced by subcutaneous injection of testosterone[20 mg/(kg·d)]for 4 weeks. Meanwhile silodosin+ BPH groups rats were administered silodosin 4 weeks[100 μg/(kg·d)]. After 4 weeks, all animals were sacrificed to examine the blood biochemical profiles, prostate volume, weight, histopathological changes, and epidermal growth factor receptor (EGFR) and B-cell chronic lymphocytic leukemia (CLL)/lymphoma 2 (BCL-2) protein expressions. Results Each group showed an increase compared to their initial body weight; however, differences in weight change between groups were not significant (P>0.05). The BPH group displayed lower glucose levels than the control group. The serum levels of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) were not significantly different among groups (P>0.05). The group treated with silodosin showed significantly lesser prostate size and weight than the testosterone-induced BPH group[volume: (0.93±0.14)cm3 vs (1.75±0.15)cm3, P<0.01; weight: (0.97±0.06)g vs (1.30±0.05)g, P<0.01]. In addition, silodosin decreased the expressions of EGFR and BCL-2 in prostate tissues (P<0.05). Conclusions These results suggest that silodosin suppress the development of BPH by inhibiting the expressions of EGFR and BCL-2. Key words: Adrenergic beta-antagonists/PD; Testosterone/AE; Prostatic hyperplasia/ET/DT