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Molecular and Histologic Evidence of Novel Erectile Dysfunction Rat Model as an Aging Atherosclerosis Model: A
Jae Heon Kim1, Ji Sung Shim2, Jong Wook Kim2
1Department of Urology, Soonchunhyang University Hospital, Soonchunhyang University College of Medicine, Seoul, Korea.
Purpose:
To validate a novel arteriogenic erectile dysfunction (ED) model with atherosclerosis (AS) based on molecular and histologic evidence induced by chronic pelvic ischemia (CPI) and determine effect of phosphodiesterase-5 inhibitor treatment.
Materials And Methods:
Twenty 16-week-old male Sprague-Dawley rats were divided into three experimental groups (Group I, untreated sham-operated rats with regular diet; Group II, CPI with cholesterol diet; Group III, CPI model with cholesterol diet and mirodenafil). Erectile function was accessed using maximum intracavernous pressure (ICP) and ICP/mean arterial pressure (MAP). Molecular changes were examined by western blot analysis using hypoxia inducible factor 1-alpha (HIF-1α), endothelial nitric oxide synthase (eNOS), and transforming growth factor beta-1 (TGF-β1) antibodies. Collagen change was evaluated by Masson's trichrome staining.
Results:
In vivo measurements of ICP and ICP/MAP in Group II were significantly lower than those in Group I (p<0.01). Smooth muscle/collagen ratio in Group II was significantly lower than that in Group I (p<0.05). After treatment with mirodenafil for four weeks, Group III showed significantly higher levels of ICP and ICP/MAP than Group II (p<0.05). Western blot analysis showed that HIF-1α and TGF-β1 levels were significantly higher in Group II whereas eNOS levels were significantly lower in Group II than those in Group I or III.
Conclusions:
A novel arteriogenic ED with AS model is successfully induced by CPI and validated based on molecular and histologic evidences.
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