Hormonal replacement has been utilized to minimize the harmful effects of hormonal imbalance in elderly men. The development and progression of
prostatic diseases and their relation to
hormone therapy is still unclear. Thus, the aim herewith was to characterize the structure and
dystroglycan molecule (DGs) reactivities in the ventral prostatic lobe from elderly rats submitted to
steroid hormone replacement. Male rats (Sprague-Dawley) were divided into one Young group and six senile groups. The Young group (YNG) (4 months old) received
peanut oil (5mL/kg, s.c.). The senile rats (10 months old) were submitted to the following treatments: Senile group (SEN) (5mL/kg
peanut oil, s.c.);
Testosterone group (TEST) (5mg/kg
testosterone cipionate, s.c.);
Estrogen group (EST) (25μg/kg 17β-
estradiol, s.c.); Castrated group (CAS) (surgical
castration); Castrated-
Testosterone (CT) (surgical
castration and treatment similar to TEST group); and Castrated-
Estrogen (CE) (surgical
castration and treatment similar to EST group). After 30 days treatment, blood samples were collected for hormonal analysis and ventral prostate samples were processed for light and transmission electron microscopies, morphometrical analysis, immunohistochemistry and Western Blotting. The results showed decreased serum
testosterone levels in the senescence and increased
testosterone and
estrogen plasmatic levels after
hormone administration in the TEST and EST groups, respectively, highlighting the
therapy efficiency. Hypertrophied stroma and inflammatory cells were verified in the SEN group. After
hormone replacement in the senescence or following
castration, atrophic epithelium, epithelial cells with clear cytoplasmic halo around the nucleus, microacini and maintenance of hypertrophied stroma were seen. Decreased DG levels were verified in the senescence. After hormonal
therapy, increased
protein levels of these molecules were observed, especially in those groups which received
estradiol. Thus, the occurrence of inflammatory cells, stromal
hypertrophy and the presence of cells with clear halo around the nucleus after hormonal
therapy probably indicated prostatic paracrine signaling imbalance, suggesting a stromal reactive microenvironment favorable to the development of glandular lesions. However, the increase of DG levels characterized positive effect of
steroid hormone replacement on the prostate in the senescence. Thus, it could be concluded that despite having positive effects on important molecules involved in the maintenance of epithelial-stromal interaction and glandular cytoarchitecture, such as DGs, hormonal
therapy enhanced structural changes associated with senescence, probably due to increased hormonal imbalance between
androgens and
estrogens in the prostatic tissue.