Abstract

To evaluate the expression of endothelial and inducible NOS in addition to the miRNA-27b in the corpus cavernosum and peripheral blood of healthy rats, diabetic rats, alcoholic rats and rats with both pathologies. Forty eight Wistar rats were divided into four groups: control (C), alcoholic (A), diabetic (D) and alcoholic-diabetic (AD). Samples of the corpus cavernosum were prepared to study protein expressions of eNOS and iNOS by immunohistochemistry and expression of miRNA-27b in the corpus cavernosum and peripheral blood. Immunohistochemistry for eNOS and iNOS showed an increase in cavernosal smooth muscle cells in the alcoholic, diabetic and alcoholic-diabetic groups when compared with the control group. Similarly, the mRNA levels for eNOS were increased in cavernosal smooth muscle (CSM) in the alcoholic, diabetic and alcoholic-diabetic groups and miRNA-27b were decreased in CSM in the alcoholic, diabetic and alcoholic-diabetic groups. The major new finding of our study was an impairment of relaxation of cavernosal smooth muscle in alcoholic, diabetic, and alcoholic-diabetic rats that involved a decrease in the nitric oxide pathway by endothelium-dependent mechanisms accompanied by a change in the corpus cavernosum contractile sensitivity.

Highlights

  • Erectile dysfunction is characterized by a persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance[1]

  • The present study aims at evaluating the gene and protein expressions of iNOS and eNOS isoforms, as well as microRNA-27b in the corpus cavernosum and in the peripheral blood of rats submitted to model of alcoholism and diabetes

  • A significant decrease in the expression of miRNA-199 was observed in the tissue of the corpus cavernosum and blood of the rats in the AD group when compared to the C group (Figure 5)

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Summary

Introduction

Erectile dysfunction is characterized by a persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance[1]. It is estimated that the overall prevalence of erectile dysfunction (ED) is approximately 20% of the male population[3]. Prevalence increases with age and comorbidities such as type II diabetes, obesity, cardiovascular diseases, hypertension, dyslipidemia, and benign prostatic hyperplasia (BPH)[5,6,7]. Nowadays it is widely accepted that the release of NO into the cavernous tissue is the most important event triggering erection; it arises as a neurotransmitter of non-adrenergic and non-cholinergic neurons (NANC) and as vasodilator derived from the endothelium, acting in order to increase intracellular levels of cGMP in the cavernous vascular smooth muscle[8-13]. Diabetics have a higher incidence of ED, probably due to vascular and neurological changes as a result of the disease, this dysfunction can occur even with normal glycemic indexes. Pathological alterations in the cavernous arteries, ultrastructural alterations in the smooth muscle cavernosa and decrease in endothelium relaxation dependent on the smooth muscle cavernosa were observed in samples of cavernous tissue of diabetic patients[14,15]

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