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Effects of Estrogen Receptor ? Stimulation in a Rat Model of Non-Bacterial Prostatic Inflammation.

ABSTRACT: There is increasing evidence showing that chronic non-bacterial prostatic inflammation is involved in the pathogenesis of benign prostatic hyperplasia (BPH) and male lower urinary tract symptoms (LUTS). It has also been reported that estrogen receptor ? (ER?) could have an immunoprotective role in prostatic tissue. Therefore, we investigated the effect of ER?-activation on not only prostatic inflammation, but also bladder overactive conditions in a rat model with nonbacterial prostatic inflammation.Male Sprague-Dawley rats (8 weeks, n?=?15) were divided into three groups: sham-saline group (n?=?5), formalin-vehicle group (n?=?5), and formalin-treatment group (n?=?5). The sham-saline group had sham operation and 50??l normal saline injected into each ventral lobe of the prostate. The formalin-vehicle group had 50??l 5% formalin injection into bilateral ventral lobes of the prostate. The formalin-treatment group was treated with 3?-Adiol (a selective ER? agonist precursor) at a dose of 3?mg/kg daily from 2 days before induction of prostatic inflammation, whereas formalin-vehicle rats received vehicle (olive oil). In each group, conscious cystometry was performed on day 28 after intraprostatic formalin injection or sham treatment. After cystometry, the bladder and prostate were harvested for evaluation of mRNA expression and histological analysis.In cystometric investigation, the mean number of non-voiding contractions was significantly greater and voiding intervals were significantly shorter in formalin-vehicle rats than those in sham-saline rats (P?

SUBMITTER: Mizoguchi S

PROVIDER: S-EPMC5968815 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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Effects of Estrogen Receptor β Stimulation in a Rat Model of Non-Bacterial Prostatic Inflammation.

Mizoguchi Shinsuke S Mori Kenichi K Wang Zhou Z Liu Teresa T Funahashi Yasuhito Y Sato Fuminori F DeFranco Donald B DB Yoshimura Naoki N Mimata Hiromitsu H

The Prostate 20170209 7

<h4>Background</h4>There is increasing evidence showing that chronic non-bacterial prostatic inflammation is involved in the pathogenesis of benign prostatic hyperplasia (BPH) and male lower urinary tract symptoms (LUTS). It has also been reported that estrogen receptor β (ERβ) could have an immunoprotective role in prostatic tissue. Therefore, we investigated the effect of ERβ-activation on not only prostatic inflammation, but also bladder overactive conditions in a rat model with nonbacterial ...[more]

PMID: 28181685

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Project description:BackgroundDutasteride administration reportedly improves lower urinary tract symptoms in patient with chronic, histologically-identified prostatic inflammation, potentially through estrogen receptor β (ERβ), activation of which has anti-inflammatory effects in the prostate tissue. Therefore, we investigated the effect of dutasteride on intraprostatic inflammatory responses and bladder activity using a rat model of chemically induced prostatic inflammation.MethodsMale Sprague-Dawley rats at 10 weeks old were used. Prostatic inflammation was induced by 5% formalin injection into ventral lobes of the prostate and saline was injected in the control group (control, n = 5). Rats with prostatic inflammation were divided into dutasteride therapy (dutasteride, n = 5) and placebo groups (placebo, n = 5). Dutasteride was administrated at a dose of 0.5 mg/kg daily from 2 days before induction of prostatic inflammation whereas placebo rats received vehicle only. Twenty-eight days later, cystometry was performed in a conscious condition to measure non-voiding contractions (NVCs), intercontraction intervals (ICI) and postvoid residual volume (RV). After cystometry, the prostate was excised for analysis of messenger RNA (mRNA) expression levels of ERα, ERβ, interleukin-1β (IL-1β), and IL-18 by quantitative polymerase chain reaction.ResultsThe mean number of NVCs was significantly greater in placebo group than that of control group without prostatic inflammation (p < .05), and ICI were significantly decreased in placebo group compared with control group (p < .05). On the contrary, there was no significant change in NVCs or ICI between control and dutasteride groups. RV was not significantly different among three groups. Gene expression levels of ERα, IL-1β, and IL-18 was significantly increased in placebo rats compared with control rats (p < .05), but not significantly different between control and dutasteride rats. On the other hand, the mRNA expression level of ERβ was significantly decreased in placebo rats (p < .05), but not in dutasteride rats, compared with control rats.ConclusionDutasteride treatment improved not only prostatic inflammation evident as increased gene expression levels in IL-1β and IL-18, but also bladder overactivity shown by increased NVCs during bladder filling. These therapeutic effects were associated with the restored expression of anti-inflammatory ERβ. Therefore, dutasteride might be effective via ERβ modulation for the treatment of prostatic inflammation in addition to its previously known, anti-androgenic effects on benign prostatic hyperplasia.

Dataset Information

Effects of Estrogen Receptor ? Stimulation in a Rat Model of Non-Bacterial Prostatic Inflammation.

Publications

Effects of Estrogen Receptor β Stimulation in a Rat Model of Non-Bacterial Prostatic Inflammation.

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