Abstract
BackgroundA decreased prostatic blood flow could be one of the risk factors for benign prostatic hyperplasia/benign prostatic enlargement. The spontaneously hypertensive rat (SHR) shows a chronic prostatic ischemia and hyperplastic morphological abnormalities in the ventral prostate. The effect of silodosin, a selective alpha1A-adrenoceptor antagonist, was investigated in the SHR prostate as a prostatic hyperplasia model focusing on prostatic blood flow.MethodsTwelve-week-old male SHRs were administered perorally with silodosin (100 μg/kg/day) or vehicle once daily for 6 weeks. Wistar Kyoto (WKY) rats were used as normotensive controls and were treated with the vehicle. The effect of silodosin on blood pressure and prostatic blood flow were estimated and then the prostates were removed and weighed. The tissue levels of malondialdehyde (MDA), interleukin-6 (IL-6), chemokine (C-X-C motif) ligand 1/cytokine-induced neutrophil chemoattractant 1 (CXCL1/CINC1), tumor necrosis factor-alpha (TNF-α), transforming growth factor beta 1 (TGF-β1), basic fibroblast growth factor (bFGF) and alpha-smooth muscle actin (α-SMA) were measured. The histological evaluation was also performed by hematoxylin and eosin staining.ResultsThere was a significant increase in blood pressure, prostate weight, prostate body weight ratio (PBR), tissue levels of MDA, IL-6, CXCL1/CINC1, TNF-α, TGF-β1, bFGF and α-SMA in the SHR compared to the WKY rat. The ventral prostate in the SHR showed the morphological abnormalities compared to the WKY rat. Prostatic blood flow was decreased in the SHR. However, treatment with silodosin significantly restored the decreased prostatic blood flow in the SHR. Moreover, silodosin normalized tissue levels of MDA, IL-6, CXCL1/CINC1, TNF-α, TGF-β1, bFGF and α-SMA, and it ameliorated ventral prostatic hyperplasia in the SHR excluding blood pressure. Silodosin decreased PBR but not prostate weight in the SHR.ConclusionsSilodosin can inhibit the progression of prostatic hyperplasia through a recovery of prostatic blood flow.
Highlights
Benign prostatic hyperplasia (BPH) is one of the most common diseases among elderly men
There was a significant increase in blood pressure, prostate weight, prostate body weight ratio (PBR), tissue levels of MDA, IL-6, CXCL1/CINC1, tumor necrosis factor-α (TNF-α), TGF-β1, basic fibroblast growth factor (bFGF) and α-SMA in the spontaneously hypertensive rat (SHR) compared to the Wistar Kyoto (WKY) rat
Silodosin can inhibit the progression of prostatic hyperplasia through a recovery of prostatic blood flow
Summary
Benign prostatic hyperplasia (BPH) is one of the most common diseases among elderly men. Epidemiological data show that approximately 50% of patients develop lower urinary tract symptoms (LUTS) due to BPH/benign prostatic enlargement (BPE) [1]. Aging and androgens are two established risk factors for the development of BPH/BPE, serum androgen levels are generally decreased in elderly males and are not correlated with prostate volume [2]. De Nuzio et al suggested that BPH related LUTS are caused by multiple factors including pelvic atherosclerosis followed by chronic ischemia of prostate, and chronic inflammation in the prostate [7]. Recent basic and clinical research suggest that prostatic inflammation could be one of the central mechanisms in the development of BPH/ BPE [9,10]. A decreased prostatic blood flow could be one of the risk factors for benign prostatic hyperplasia/benign prostatic enlargement. The effect of silodosin, a selective alpha1A-adrenoceptor antagonist, was investigated in the SHR prostate as a prostatic hyperplasia model focusing on prostatic blood flow
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