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Rat Prostate (rat + prostate)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Vitamin D and androgen regulation of prostatic growth

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2003
Eddy S. Leman
Abstract Vitamin D has been reported to inhibit the growth of prostate cancer cells and model systems. In this study, we examined the interaction between 1,25-dihydroxyvitamin D3 (1,25 D) in the presence or absence of endogenous testosterone on the growth and development of the adult rat prostate. Male Sprague,Dawley rats (165 days old) were either kept intact or castrated. Seven days after castration, the rats were treated with vehicle (control) or 1,25 D for 3 weeks and then sacrificed. Both ventral and dorsal lateral prostates were harvested; whole tissue lysates were collected and AR and VDR protein levels were analyzed by immunoblot analyses. Administration of 1,25 D in the intact animals decreased the prostatic size by 40%, compared to control animals, whereas 1,25 D did not influence the size of the prostate in castrated rats. 1,25 D administration in intact groups also increased both the AR and VDR protein levels by ,twofold, whereas in castrated groups, 1,25 D only increased the AR protein level by 1.5,2.5-fold. 1,25 D in the presence of endogenous testosterone inhibits prostatic growth, whereas 1,25 D in the absence of endogenous testosterone does not affect prostatic growth. The growth inhibitory activity of 1,25 D in the presence of testosterone may be mediated through the ligand activated AR and VDR pathways. These studies may reveal important information about the potential efficacy of 1,25 D as well as hormonal status in understanding the development of prostate diseases. J. Cell. Biochem. 90: 138,147, 2003. © 2003 Wiley-Liss, Inc. [source]

cGMP-enhancing- and ,1A/,1D -adrenoceptor blockade-derived inhibition of Rho-kinase by KMUP-1 provides optimal prostate relaxation and epithelial cell anti-proliferation efficacy

THE PROSTATE, Issue 13 2007
Chi-Ming Liu
Abstract Background Soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) and Rho kinase (ROCK2) pathways are important in the regulation of prostate smooth muscle tone. This study is aimed to examine the relaxation activities of a sGC activator and PDE5A/ROCK2 inhibitor KMUP-1 in rat prostate and associated anti-proliferation activity in human prostatic epithelial cells. Methods The action characteristics of KMUP-1 were identified by isometric tension measurement, receptor binding assay, Western blotting and radioimmunoassay in rat prostate. Anti-proliferation activity of KMUP-1 in human prostatic epithelial PZ-HPV-7 cells was identified using flow cytometry and real time QRT-PCR. Results KMUP-1 inhibited phenylephrine-induced contractility in a concentration-dependent manner. KMUP-1 possessed potent ,1A/,1D -adrenoceptor binding inhibition activity, increased cAMP/cGMP levels and increased the expression of sGC, PKG, and PKA protein in rat prostate. Moreover, KMUP-1 inhibited phenylephrine-induced ROCK2 expression. KMUP-1 inhibited cell growth, arrested the cell cycle at G0/G1 phase and increased the expression of p21 in PZ-HPV-7 cells. Conclusions These results broaden our knowledge of sGC/cGMP/PKG and ROCK2 regulation on the relaxation and proliferation of prostate, which may help in the design of benign prostate hyperplasia (BPH) therapies that target these signaling pathways. KMUP-1 possesses the potential benefit in the treatment of BPH by its ,1A/,1D -adrenoceptor blockade, sGC activation, inhibition of PDE5A and ROCK2 and p21 protein enhancement, leading to attenuation of the smooth muscle tone and the proliferation of epithelial PZ-HPV-7 cells. The synergistic contribution of these pathways by KMUP-1 may benefit BPH patients with lower urinary tract symptoms. Prostate 67: 1397,1410, 2007. © 2007 Wiley-Liss, Inc. [source]

Effects of two new steroids and cyproterone on some biomarkers of oxidative stress and serotonergic system on rat prostate and brain

ANDROLOGIA, Issue 1 2009
G. D. Calderón
Summary The purpose of this study was to evaluate the effect of cyproterone acetate (CPA, A) compared with new synthetic steroids 3,-acetoxy-5,6-epoxy-16-pregnen-20-one (B) and 17,-hydroxy-16,-methyl-1,4,6-pregnatriene-3,20-dione (C) in rat prostate and brain. Groups of animals were treated either with A, B or C (4 mg kg,1 day,1) by the intraperitoneal route for 5 days. Levels of reduced glutathione (GSH), 5-hydroxy-indole acetic acid (5-HIAA), lipid peroxidation (as thiobarbituric acid reactive substances, TBARS) and the activities of Na+, K+ - and total ATPases were assayed in prostate and brain for each group of animals including a control group. No appreciable changes were shown in Na+, K+ -ATPase and total ATPases and TBARS on prostate and brain of rats that received A, B and C steroids. However, the levels of GSH and 5-HIAA decreased significantly (P < 0.05) in both tissues for the steroids assayed. It is concluded that CPA and the homologues B and C steroids induce changes in the levels of GSH and serotonin in rat prostate and brain. [source]

Survivin mediates prostate cell protection by HIF-1, against zinc toxicity

THE PROSTATE, Issue 11 2010
Young-Joo Yun
Abstract BACKGROUND The prostate contains extremely high concentrations of zinc, but survives and grows without apparent injury. This begs the question as to how prostate cells avoid the toxic effects of zinc. In a previous study, the authors found that; HIF-1, is expressed concomitantly with the accumulation of zinc in the epithelial cells of normal rat prostates, the zinc ion stabilizes HIF-1, in prostate cells, and that HIF-1, protects prostate cells from zinc toxicity. In the present study, the authors addressed the mechanism responsible for the protective effect of HIF-1, in a high zinc environment. METHODS Immunofluorescent staining, immunoblotting, reverse transcription-polymerase chain reaction, reporter assay, and cell cycle analysis. RESULTS Survivin was induced by ZnCl2 in a HIF-1 dependent manner in both DU-145 and PNT2 prostate cells. Furthermore, HIF-1 induced survivin expression at the transcriptional level and the induction of survivin was abolished by HIF-1, knock-down. In addition, HIF-1-dependent survivin overexpression promoted prostrate cell survival and prevented cell arrest in the presence of high zinc concentrations, and si-survivin transfected cells under zinc rich conditions contained markedly higher levels of cleaved caspase-9 and PARP than si-con transfected cells. Finally, survivin expression patterns well matched rat prostate proliferation statuses. CONCLUSION Under zinc rich conditions, prostate epithelial cells HIF-1-dependently express survivin, which promotes prostate cell proliferation, and prevents apoptosis and cell cycle arrest. Accordingly, the HIF-1,-survivin pathway appears to facilitate prostate cell survival and growth in zinc rich environments, and this pathway could be a therapeutic target for the treatment of prostate hyperplasia. Prostate 70: 1179,1188, 2010. © 2010 Wiley-Liss, Inc. [source]