Romanian Society of Pharmaceutical Sciences
 

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THE MITIGATING EFFECT OF AZILSARTAN ON INDUCED BENIGN PROSTATIC HYPERPLASIA IN RATS THROUGH WNT/β-CATENIN/ PPAR-γ AND ANGIOTENSIN-II AXIS

ALI HUSSEIN JASIM 1 , AHMED RAHMAH ABU-RAGHIF 1, HAYDER S RWAYYIH 2 , MOHAMMED TH. S AL-ZUBAIDI 3, ZEENA AYAD HUSSEIN 1*

1 Department of Pharmacology, College of Medicine, Al-Nahrain University, Baghdad, Iraq
2 Physiology, Biochemistry and Pharmacology Department, College of Veterinary Medicine, University of Baghdad, Baghdad, Iraq
3 Department of Parasitology, College of Veterinary Medicine, University of Baghdad, Baghdad, Iraq

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Benign prostatic hyperplasia (BPH) is a common and disruptive health problem among elderly men. This study investigated the effect of azilsartan on BPH and its mechanisms. This study investigated the effectiveness of azilsartan medoxomil in preventing testosterone propionate (TP)-induced benign prostatic hyperplasia in rats. The experiment included 40 male Wistar rats. Animals were randomly assigned to four groups. The healthy (control) group received the vehicle orally and subcutaneously daily. The Induced (TP) group was given only 3 mg/kg testosterone propionate SC daily for 28 days. The therapy groups (TP + FIN and TP + AZ) were given testosterone propionate, finasteride 5 mg/kg/day, and azilsartan medoxomil 5 mg/kg/day orally. Prostate tissue samples were collected from euthanised animals on day 30 to evaluate prostatic index, histology, hyperplastic markers, inflammatory markers and PPAR-γ gene expression. Azilsartan significantly lowers prostate index compared to the induced (TP) group (P < 0.0001). The treatment normalised BPH markers, including 5α-reductase type 2 enzyme, dihydrotestosterone, TGF-β, VEGF, IL-6 and PCNA (P < 0.0001), while downregulating Ang II receptors and upregulating PPAR γ receptors. The agent reduced β-catenin levels in the tissue. AZ can prevent BPH in rats by decreasing cellular proliferation through activation of the PPAR-γ pathway. It also interferes with renin-angiotensin, prostatic androgen and Wnt pathways.