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Improvement in erectile function in a rat model of high cholesterol diet‐induced atherosclerosis by atorvastatin in a manner that is independent of its lipid‐lowering property
Author(s) -
Zhang Z.,
Tang L.,
Yu W.,
Chen Y.,
Dai Y.t.
Publication year - 2017
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.12789
Subject(s) - atorvastatin , enos , endocrinology , medicine , erectile dysfunction , oxidative stress , sildenafil , nitric oxide , hmg coa reductase , lipid profile , nitric oxide synthase , chemistry , cholesterol , pharmacology , biochemistry , reductase , enzyme
Summary The purpose of the present study is to explore the effects of a lipid‐lowering drug atorvastatin, a three‐hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase inhibitor, in the treatment of erectile dysfunction (ED) in a rat model of atherosclerosis (AS) and the possible mechanisms underneath. A high‐cholesterol diet was administrated to Sprague‐Dawley rats in an attempt to induce an ASED model, which was later confirmed by abdominal aorta histopathology and erectile function evaluation. ASED rats were further assigned to non‐treatment group, atorvastatin low‐dose treatment group (5 mg kg −1 day −1 ), high‐dose group (10 mg kg −1 day −1 ) and sildenafil (1.5 mg kg −1 day −1 ) treatment group. Lipid profile, erectile function, oxidative stress biochemical markers, endothelial nitric oxide synthase (eNOS) and extracellular superoxide dismutase (SOD EX ) mRNA expression were evaluated after 8‐week treatment duration. Erectile function was impaired in AS rat model, which was preserved in atorvastatin and sildenafil intervention groups. The oxidative stress biochemical markers were attenuated, while eNOS and SOD EX mRNA expression were restored in atorvastatin and sildenafil groups, which were found to be involved in ED pathogenesis. However, the lipid profile remained unaltered in the treatment group, and it was elevated in ASED rats. This kind of lipid‐lowering agent, or atorvastatin, has the utilisation potential in ASED treatment, even before lipid profiles altered. This effect on erectile function preservation of atorvastatin was attributed to its preservation of endothelial function, possibly through amelioration of oxidative stress and improvement in eNOS expression.