• Journal of Yeungnam Medical Science
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• v.23 no.1
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• pp.62-70
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• 2006

Background: Benign prostatic hyperplasia (BPH) is the most common benign tumor in older men; the etiology of this disease remains poorly understood. Testosterone and dihydrotestosterone (DHT) both act as androgen via a single androgen receptor. Testosterone is converted to DHT by $5{\alpha}$-reductase in prostatic stromal cells. Progesterone has been reported to inhibit DHT conversion; howevwe, its effect on prostatic stromal cells remains to be elucidated. Materials and Methods: In this experiment, we investigated the effect of progesterone on androgen receptor expression induced by DHT. We also tested the effect of progesterone on cyclooxygenase-2 (COX-2) expression, as well as prostate stromal cell proliferation using the cell count kit-8. Results: Progesterone did not cause an increase of prostate stromal cell proliferation. The mRNA expression of the androgen receptor and COX-2 were not changed by progesterone; the expressions of androgen receptor and COX-2 proteins were decreased by progesterone in prostate stromal cells. Conclusion: These results suggest that in prostate stromal cells, progesterone decreases androgen receptor protein expression, which results in decrement of COX-2 protein expression. This effect might be mediated by post-transcriptional regulation.

• Parasites, Hosts and Diseases
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• v.61 no.1
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• pp.2-14
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• 2023

Trichomonas vaginalis is a flagellated protozoan that causes trichomoniasis, a common nonviral sexually transmitted infection. T. vaginalis infection is asymptomatic in most infected men but can lead to chronic infection. The inflammatory response to chronic T. vaginalis infection may contribute to prostatic diseases, such as prostatitis and benign prostatic hyperplasia (BPH); however, studies on the relationship between T. vaginalis infection and prostate diseases are scarce. In this review, we discuss evidence from our studies on the involvement of T. vaginalis in the pathogenesis of prostate diseases, such as prostatitis and BPH. Studies of prostatitis have demonstrated that the attachment of T. vaginalis trophozoite to prostate epithelial cells (PECs) induces inflammatory cytokine production and inflammatory cell migration, leading to prostatitis. T. vaginalis also causes pathological changes, such as inflammatory cell infiltration, acinar changes, interstitial fibrosis, and mast cell infiltration, in prostate tissues of infected rats. Thus, T. vaginalis is considered an infectious agent that triggers prostatitis. Meanwhile, studies of prostatic hyperplasia revealed that mast cells activated by T. vaginalis-infected prostate cells secreted inflammatory mediators, such as β-hexosaminidase and tryptase, which promoted proliferation of prostate stromal cell (PSC). Moreover, interleukin-6 produced by proliferating PSCs induced the multiplication of BPH-1 epithelial cells as a result of stromal-epithelial interaction, suggesting that the proliferation of T. vaginalis-infected prostate cells can be induced through crosstalk with mast cells. These collective findings suggest that T. vaginalis contributes to the progression of prostatitis and prostatic hyperplasia by creating an inflammatory microenvironment involving PECs and PSCs.

• Parasites, Hosts and Diseases
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• v.59 no.3
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• pp.235-249
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• 2021

Leptin is a type of adipokine mainly produced by adipocytes and reported to be overproduced in prostate cancer. However, it is not known whether it stimulates the proliferation of prostate cells. In this study, we investigated whether benign prostatic hyperplasia epithelial cells (BPH-1 cells) infected with Trichomonas vaginalis induced the proliferation of prostate cells via a leptin signaling pathway. To investigate the effect of crosstalk between adipocyte leptin and inflamed epithelial cell in proliferation of prostate cells, adipocytes 3T3-L1 cells were incubated in conditioned medium of BPH-1 cells infected with T. vaginalis (T. vaginalis-conditioned medium, TCM), and then the adipocyte-conditioned medium (ATCM) was identified to cause proliferation of prostate cells. BPH-1 cells incubated with live T. vaginalis released pro-inflammatory cytokines, and conditioned medium of these cells caused migration of adipocytes. When prostate stromal cells and BPH-1 cells were incubated with adipocyte conditioned medium containing leptin, their growth rates increased as did expression of the leptin receptor (known as OBR) and signaling molecules such as JAK2/STAT3, Notch and survivin. Moreover, blocking the OBR reduced this proliferation and the expression of leptin signaling molecules in response to ATCM. In conclusion, our findings show that inflamed BPH-1 cells infected with T. vaginalis induce the proliferation of prostate cells through leptin-OBR signaling. Therefore, it is likely that T. vaginalis contributes to prostate enlargement in BPH via adipocyte leptin released as a result of inflammation of the prostate.

• Korean Journal of Radiology
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• v.2 no.3
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• pp.159-163
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• 2001

Objective: The purpose of this study is to correlate the findings of peripheral hypoechoic rim, seen at transrectal ultrasonography (TRUS) in chronic prostatitis patients, with the histopthologic findings. Materials and Methods: Seven patients with pathologically proven chronic prostatitis were involved in this study. The conspicuity of the peripheral hypoechoic prostatic rim, seen at TRUS, was prominent and subtle, and to determine its histopathologic nature, the microscopic findings were reviewed. Results: In five of seven cases (71%), TRUS demonstrated a prominent peripheral hypoechoic rim. Microscopic examination revealed that inflammatory cell infiltration of prostatic glandular tissue was severe in three cases (42.9%), moderate in two (28.6%), and minimal in two (28.6%). In all seven cases, the common histopathologic findings of peripheral hypoechoic rim on TRUS were loose stromal tissues, few prostatic glands, and sparse infiltration by inflammatory cells. Conclusion: The peripheral hypoechoic rim accompanying prostatic inflammation and revealed by TRUS reflects a sparsity of prostate glandular tissue and is thought to be an area in which inflammatory cell infiltration is minimal.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.4
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• pp.507-515
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• 2014

Benign prostatic hyperplasia (BPH), which is commonly found in aging men, is characterized by hyperplasia of prostatic stromal and epithelial cells beginning in the periurethral zone of the prostate. The prevalence of BPH increases in an age-dependent manner. Here, we investigated the protective effects of unripe Rubus occidentalis extracts (UROE) on BPH development using a prostate cancer cell line and testosterone-induced BPH rat model. Experiments using an established hormone-dependent prostate cancer cell line (LNCaP) showed that UROE treatment significantly decreased expression of androgen-related genes, including androgen receptor (AR), prostate specific antigen (PSA), and 5-alpha reductase 2, but not 5-alpha reductase 1, which was also observed in flutamide-treated cells. Further, AR and PSA gene expression was reduced by UROE treatment under androgen-stimulated conditions using dihydrotestosterone (DHT). BPH animals displayed elevated prostate weights. However, UROE as well as finasteride treatment significantly reduced prostate weights and DHT levels compared to testosterone-induced BPH animals. Histopathological analysis also showed that UROE treatment suppressed testosterone-induced prostatic hyperplasia. Taken together, the results suggest that UROE may effectively inhibit the development of BPH and thus may be a useful agent in BPH treatment.

• The Journal of Internal Korean Medicine
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• v.31 no.3
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• pp.457-466
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• 2010

Objective : In benign prostatic hyperplasia, dihydrotestosterone acts as a potent cellular androgen and promotes prostate growth. Inhibiting enzyme $5{\alpha}$-reductase that is involved in the conversion of testosterone to the active form dihydrotestosterone reduces this excessive prostate growth. The mechanism on benign prostatic hyperplasia is substantiating evidence to support the clinical value in the evaluation of therapeutic efficacy. In this study, we investigated the effects of Lygodium japonicum on cyto-pathological alterations and expression of $5{\alpha}$-reductase in the rat model of benign prostatic hyperplasia induced by castration and testosterone treatment. Methods : Sprague-Dawley rats were treated with testosterone after castration for induction of experimental benign prostatic hyperplasia, which is similar to human benign prostatic hyperplasia in histopathological profiles. Lygodium japonicum as an experimental specimen, and finasteride as a positive control, were administered orally. The prostates were evaluated by histopathological changes and testosterone levels. Also, the prostates were observed by hematological alterations of AST, ALT, ${\gamma}$-GTP, BUN and creatinine. Results : The rats treated with Lygodium japonicum showed a diminished range of luminal cell and duct epithelial cell damage. The stromal elements and connective tissue proliferation of Lygodium japonicum treated group as compared to the control group decreased. Conclusions : These findings suggest that Lygodium japonicum may protect the glandular epithelial cells. We concluded that Lygodium japonicum could be a useful remedy agent for treating the benign prostatic hyperplasia.

• Journal of Life Science
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• v.29 no.6
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• pp.705-711
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• 2019

Benign prostatic hyperplasia (BPH) is the most common urogenital disorder in men, benign tumor and is a typical disease deteriorating the quality of old men's lives, and its prevalence increases with age. Though the molecular pathogenesis of BPH has not yet been clearly revealed, it is known that the variation and aging of the endocrine including sex hormone may cause BPH. Especially the hypertrophy of the prostate cell by the formation of the excessive dihydrotestosterone (DHT) is estimated to cause BPH. If testosterone exists excessively in blood, a lot of DHT is produced in prostate by $5{\alpha}-reductase$. Thus, in this study we tried to analyze haematological change and histopathological change by using the model rat with BPH caused by hypodermic injection of testosterone to prove the effect of Houttuynia cordata extracts on BPH. Rats were divided into four experimental groups: no treatment group (N), the testosterone injection and D.W treatment group (DO), the testosterone injection and Houttuynia cordata treatment group (HO) and testosterone injection and finasteride treatment group (FO). Prostate weight, volume and weight ratio in the HO and FO groups were significantly lower than the DO group. Testosterone and DHT levels in the HO group were significantly lower than the DO group. The HO and FO groups showed trophic symptoms and were lined by flattened epithelial cells, thus, the stromal proliferation is relatively low as compared to the DO group. These results suggest that Houttuynia cordata may control benign prostatic hyperplasia.

• Korean Journal of Microbiology
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• v.43 no.3
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• pp.151-158
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• 2007

The possibility of inadvertent introduction of therapeutic gene expressing viral vectors has raised safety concerns about germ-line infection. Particularly, for indications such as prostate cancer and ovarian cancer, the proximity of the point of viral administration to organs of the reproductive system raises concerns regarding inadvertent germ-line transmission of genes carried by the virus vector. To evaluate the safety of in vivo adenovirus mediated gene transfer, we explored the biodistribution, persistance and potential germ-line transmission of p53-expressing adenovirus (Ad-CMV-p53). Both male and female Balb/c mice were injected with $1{\times}10^9$ PFU of Ad-CMV-p53. The PCR analysis showed that there were detectable vector sequences in liver, kidney, spleen, seminal vesicle, epididymis, prostate, ovary, and uterus. The RT-PCR analysis for detecting inserted gene, p53 showed that Ad-CMV-p53 viral RNA were present in spleen, prostate and ovary. Direct injected male and female mice of adenovirus vector into testis and ovary were mated and their of offspring were evaluated for germ-line transmission of the adenoviral vector. The PCR and RT-PCR analysis showed no evidence of germline transmission, although vector sequences were detected in DNA extracted from gonadal tissues. Real-time PCR result confirmed a significant decrease of adenovirus in gonad tissues 1 week after injection. We have also analysed the cell specific localization of viral DNA in gonad tissues by using in-situ PCR. Positive signals were detected in interstitial tissue but not in seminiferous tubule in sperm. In the case of ovary, adenovirus signal were localized to the stromal tissue, but no follicular signals were observed. Together, these data provide strong evidence that the risk of the Inadvertent germ-line transmission of vector sequences following intraperitoneal or direct injection into genito-urinary system of adenovirus is extremely low.