Molecular biology reports · 2026
The interplay of bosentan and finerenone in amelioration of cardiac dysfunction within benign prostatic hyperplasia in rats.
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Refaie Marwa Monier Mahmoud, Hasan Asmaa A, Muhammed Asmaa A, Ibrahim Randa Ahmed, Hassan Eman Abdel Naby, Fathy Enas, Soliman Aml Mohamed, Sherkawy Hoda S, Beshay Olivia N, Alam-Eldin Ahmed Amr, Ahmed Ahmed, Elsayed Samar Hisham, Habib Heba A
Аннотация
OBJECTIVES: Benign prostatic hyperplasia (BPH) is a widespread urological clinical case in aged men associated with troublesome lower urinary tract symptoms and cardiac dysfunction, but its medical treatment is still insufficient. Thus, searching for more effective medical regimens is an essential target. We tried in current experiment to explore the role of bosentan (BOS) and/or finerenone (FIN) in this lesion.
METHODS: BPH was adequately induced using testosterone propionate (TP) in a dose of (5 mg/kg/day) for 28 days of subcutaneous injection and an oral administration of BOS (50 mg/kg/day) and/or FIN (10 mg/kg/day) for 10 days.
RESULTS: We found typical histopathological changes of BPH, increased serum dihydrotestosterone (DHT), prostatic specific antigen (PSA), cardiac enzymes, tissue malondialdehyde (MDA), aldosterone, endothelin-A, nuclear factor kappa b (NF-κB), and proliferating cell nuclear antigen (PCNA). However, significant decreases in total antioxidant capacity (TAC), reduced glutathione (GSH), and caspase-3. The histological findings were augmented by special staining techniques, immunohistochemical and morphometric studies. There are histopathological alternations as the hyperplastic nodules in the prostate's transition zone expand, and the prostatic urethra was compressed, lengthened and distorted. Interestingly the co-administration of BOS and/or FIN significantly improved BPH induced changes. This is mostly attributed to its ability in modulating endothelin receptors by BOS, aldosterone receptors by FIN, improved the histopathological changes with anti-oxidant, anti-inflammatory, anti-fibrotic, antiproliferative, and apoptotic properties.
CONCLUSIONS: BOS and/or FIN showed a significant ameliorative effect in BPH.
METHODS: BPH was adequately induced using testosterone propionate (TP) in a dose of (5 mg/kg/day) for 28 days of subcutaneous injection and an oral administration of BOS (50 mg/kg/day) and/or FIN (10 mg/kg/day) for 10 days.
RESULTS: We found typical histopathological changes of BPH, increased serum dihydrotestosterone (DHT), prostatic specific antigen (PSA), cardiac enzymes, tissue malondialdehyde (MDA), aldosterone, endothelin-A, nuclear factor kappa b (NF-κB), and proliferating cell nuclear antigen (PCNA). However, significant decreases in total antioxidant capacity (TAC), reduced glutathione (GSH), and caspase-3. The histological findings were augmented by special staining techniques, immunohistochemical and morphometric studies. There are histopathological alternations as the hyperplastic nodules in the prostate's transition zone expand, and the prostatic urethra was compressed, lengthened and distorted. Interestingly the co-administration of BOS and/or FIN significantly improved BPH induced changes. This is mostly attributed to its ability in modulating endothelin receptors by BOS, aldosterone receptors by FIN, improved the histopathological changes with anti-oxidant, anti-inflammatory, anti-fibrotic, antiproliferative, and apoptotic properties.
CONCLUSIONS: BOS and/or FIN showed a significant ameliorative effect in BPH.