scholarly journals Extracts of Phyllostachys pubescens Leaves Represses Human Steroid 5-Alpha Reductase Type 2 Promoter Activity in BHP-1 Cells and Ameliorates Testosterone-Induced Benign Prostatic Hyperplasia in Rat Model

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 884
Author(s):  
Kwang Hoon Song ◽  
Chang-Seob Seo ◽  
Won-Kyung Yang ◽  
Hyun-O Gu ◽  
Ki-Joong Kim ◽  
...  
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Mrna Expression ◽  
Rat Model ◽  
Promoter Activity ◽  
Prostatic Hyperplasia ◽  
Human Prostate ◽  
Phyllostachys Pubescens ◽  
Prostate Cell ◽  
Srd5a2 Gene

Benign prostatic hyperplasia (BPH) is the most common symptomatic abnormality of the human prostate characterized by uncontrolled proliferation of the prostate gland. In this study, we investigated the effect of bamboo, Phyllostachys pubescens, leaves extract (PPE) on human 5α-reductase type 2 (SRD5A2) gene promoter activity in human prostate cell lines and the protective effect of PPE on a testosterone-induced BPH rat model. PPE repressed human SRD5A2 promoter activity and its mRNA expression. The rats treated with PPE for 4 weeks showed a significantly attenuated prostate weight compared to vehicle control. PPE-treated rats also showed reduced serum dihydrotestosterone, testosterone, prostate-specific antigen, and SRD5A2 levels by testosterone injection. Quantitative real-time polymerase chain reaction showed that PPE treatment significantly decreased mRNA expression of SRD5A2, androgen receptor (AR), proliferating cell nuclear antigen (PCNA), and fibroblast growth factor 2 compared with the vehicle-treated, testosterone-injected rats in the prostate. Furthermore, PPE treatment showed reduced AR, PCNA, and tumor necrosis factor alpha expression in the prostate via immunohistofluorescence staining. In conclusion, oral administration of PPE prevented and inhibited the development and progression of enlarged prostate lesions in testosterone-induced animal models through various anti-proliferative and anti-inflammatory pharmacological effects and induced suppression of SRD5A2 gene expression.

scholarly journals Effect of Paecilomyces tenuipes Extract on Testosterone-Induced Benign Prostatic Hyperplasia in Sprague–Dawley Rats

2019 ◽  
Vol 16 (19) ◽  
pp. 3764 ◽  
Author(s):  
Choi ◽  
Kim ◽  
Fan ◽  
Tang ◽  
Hwang ◽  
...  
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Rat Model ◽  
Testosterone Propionate ◽  
Inhibitory Effect ◽  
Prostatic Hyperplasia ◽  
Control Group ◽  
Lncap Cells ◽  
Prostate Cell ◽  
Expression Levels ◽  
Prostate Size

: Benign prostatic hyperplasia (BPH) is one of the major public health concerns, which has a high prevalence rate and causes significant decline in men's quality of life. BPH is highly related to sexual hormone metabolism and aging. In particular, dihydrotestosterone (DHT), to which testosterone is modified by 5α-reductase (5AR), has a significant effect on BPH development. DHT binds to an androgen receptor (AR) and steroid receptor coactivator 1 (SRC-1); then, it induces the proliferation of a prostate cell and expression of prostate specific antigen (PSA). Paecilomyces tenuipes (P. tenuipes) is a mushroom that has been popularized by the artificial cultivation of fruiting bodies based on silkworms by researchers from the Republic of Korea. In a previous study, we identified the effect of PE on PSA mRNA expression in LNCaP cells. This suggests that PE may have an inhibitory effect on androgen signaling. Therefore, we confirmed the expression of androgen signaling-related factors, such as AR, SRC-1, and PSA in LNCaP. Furthermore, we confirmed the androgen signaling inhibitory effect of PE using the testosterone propionate (TP)-induced BPH rat model. A BPH rat model was established with a four-week treatment of daily subcutaneous injections of testosterone propionate (TP, 3 mg/kg) dissolved in corn oil after castration. The rats in the treatment group were orally gavaged P. tenuipes extract (PE), finasteride (Fi), or saw palmetto extract (Saw) with TP injection. DHT induced an increase in the expression levels of AR, SRC-1, and PSA proteins in LNCaP cells. On the contrary, the PE treatment reduced the expression levels. In vivo, the BPH group showed an increase in prostate size compared with the control group. The PE gavaged group showed a decrease in prostate size compared with the BPH group. In addition, the protein expressions of AR, 5AR2, and PSA were significantly lower in the PE gavaged group than BPH group in prostate tissue. These results suggest the beneficial effects of PE on BPH via the modulation of AR signaling pathway.

scholarly journals Transcript Profiling of the Androgen Signal in Normal Prostate, Benign Prostatic Hyperplasia, and Prostate Cancer

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5806-5816 ◽  
Author(s):  
David R. Bauman ◽  
Stephan Steckelbroeck ◽  
Donna M. Peehl ◽  
Trevor M. Penning
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Stromal Cells ◽  
Cell Types ◽  
Prostatic Hyperplasia ◽  
Human Prostate ◽  
Rt Pcr ◽  
Retinol Dehydrogenase ◽  
Normal Prostate ◽  
Androgen Ablation

Human prostate adenocarcinoma (CaP) and benign prostatic hyperplasia (BPH) have epithelial and stromal cell origins, respectively. To determine whether the androgen signal is processed differently in these cell types the expression of transcripts for enzymes that control ligand access to the androgen receptor (AR) were measured. Transcripts for type 2 5α-reductase, ketosteroid reductases [aldo-keto reductase (AKR)1C1-AKR1C4], the major oxidative 3α-hydroxysteroid dehydrogenase (HSD) retinol dehydrogenase (RODH)-like 3α-HSD (RL-HSD) and nuclear receptors [AR, estrogen receptor (ER)α, and ERβ] were determined in whole human prostate and in cultures of primary epithelial cells (PEC) and primary stromal cells (PSC) from normal prostate, CaP and BPH by real-time RT-PCR. Normal PEC (n = 14) had higher levels of AKR1C1 (10-fold, P < 0.001), AKR1C2 (115-fold, P < 0.001) and AKR1C3 (6-fold, P < 0.001) than normal PSC (n = 15), suggesting that reductive androgen metabolism occurs. By contrast, normal PSC had higher levels of AR (8-fold, P < 0.001) and RL-HSD (21-fold, P < 0.001) than normal PEC, suggesting that 3α-androstanediol is converted to 5α-dihydrotestosterone to activate AR. In CaP PEC (n = 14), no significant changes in transcript levels vs. normal PEC were observed. In BPH PSC (n = 21) transcripts for AR (2-fold, P < 0.001), AKR1C1 (4-fold, P < 0.001), AKR1C2 (10-fold P < 0.001), AKR1C3 (4-fold, P < 0.001) and RL-HSD (3-fold, P < 0.003) were elevated to increase androgen response. Differences in the AR:ERβ transcript ratios (eight in normal PEC vs. 280 in normal PSC) were maintained in PEC and PSC in diseased prostate. These data suggest that CaP may be more responsive to an ERβ agonist and BPH may be more responsive to androgen ablation.

scholarly journals NELL2 Modulates Cell Proliferation and Apoptosis via ERK Pathway in the Development of Benign Prostatic Hyperplasia

2021 ◽  
Author(s):  
Jianmin Liu ◽  
Daoquan Liu ◽  
Xueneng Zhang ◽  
Yan Li ◽  
Xun Fu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Benign Prostatic Hyperplasia ◽  
Cell Apoptosis ◽  
Prostatic Hyperplasia ◽  
Human Prostate ◽  
Immunofluorescent Staining ◽  
Erk Pathway ◽  
Prostate Cell ◽  
Mesenchymal Transition ◽  
Dependent Cell

Benign prostatic hyperplasia (BPH) is a quite common illness but its etiology and mechanism remain unclear. Neural epidermal growth factor-like like 2 (NELL2) plays multifunctional roles in neural cell growth and is strongly linked to the urinary tract disease. Current study aims to determine the expression, functional activities and underlying mechanism of NELL2 in BPH. Human prostate cell lines and tissues from normal human and BPH patients were utilized. Immunohistochemical staining, immunofluorescent staining, RT-PCR and Western-blotting were performed. We further generated cell models with NELL2 silenced or overexpressed. Subsequently, proliferation, cycle, and apoptosis of prostate cells were determined by CCK-8 assay and flow cytometry analysis. The epithelial-mesenchymal transition (EMT) and fibrosis process were also analyzed. Our study revealed that NELL2 was upregulated in BPH samples and localized in the stroma and the epithelium compartments of human prostate tissues. NELL2 deficiency induced a mitochondrial-dependent cell apoptosis, and inhibited cell proliferation via phosphorylating ERK1/2 activation. Additionally, suppression of ERK1/2 with U0126 incubation could significantly reverse NELL2 deficiency triggered cell apoptosis. Consistently, overexpression of NELL2 promoted cell proliferation and inhibited cell apoptosis. However, NELL2 interference was observed no effect on EMT and fibrosis process. Our novel data demonstrated that upregulation of NELL2 in the enlarged prostate could contribute to the development of BPH through enhancing cell proliferation and inhibited a mitochondrial-dependent cell apoptosis via the ERK pathway. The NELL2-ERK system might represent an important target to facilitate the development of future therapeutic approaches in BPH.

Anti-proliferation effects of Cistanches salsa on the progression of benign prostatic hyperplasia

2016 ◽  
Vol 94 (1) ◽  
pp. 104-111 ◽  
Author(s):  
Eunjin Jeon ◽  
Kyung-Sook Chung ◽  
Hyo-Jin An
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Mrna Expression ◽  
Prostate Gland ◽  
Prostatic Hyperplasia ◽  
Prostate Tissue ◽  
Expression Levels ◽  
Prostate Weight ◽  
Related Proteins

Cistanche salsa has been used in traditional medicine for the treatment of kidney deficiency, neurasthenia, sexual dysfunction diseases, and benign prostatic hyperplasia (BPH). The aim of this study was to investigate the mechanism by which C. salsa extract (CSE) elicits an anti-proliferative effect on the prostate tissue of BPH-induced rats. The effects of CSE on BPH were evaluated in terms of prostate weight, production of serum dihydrotestosterone (DHT), and the mRNA expression of 5α-reductase type 1 and type 2 in the prostate tissue of BPH-induced rats. In addition, hematoxylin and eosin (H&E) staining was performed for histological examination of prostate gland morphology, and protein expression levels in prostate tissue were investigated by western blot analysis. CSE treatment decreased prostate weight, serum DHT concentration, and the mRNA expression of 5α-reductase type 1 and type 2 in prostate tissue of BPH-induced rats. In addition, CSE treatment suppressed cell proliferation by regulating the expression levels of inflammatory-related proteins (inducible nitric oxide synthase and cyclooxygenase 2) and apoptosis-associated proteins (caspase-3 and Bcl-2 family proteins). CSE may be a potential therapeutic candidate for BPH owing to its ability to regulate the expression of inflammatory and apoptosis-related proteins.

Localization of angiotensin-converting enzyme in the human prostate: pathological expression in benign prostatic hyperplasia

2001 ◽  
Vol 195 (5) ◽  
pp. 571-579 ◽  
Author(s):  
Labrini Nassis ◽  
Albert G. Frauman ◽  
Mitsuru Ohishi ◽  
Jialong Zhuo ◽  
David J. Casley ◽  
...  
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Angiotensin Converting Enzyme ◽  
Prostatic Hyperplasia ◽  
Human Prostate ◽  
Converting Enzyme

scholarly journals Ghrelin Aggravates Prostate Enlargement in Rats with Testosterone-Induced Benign Prostatic Hyperplasia, Stromal Cell Proliferation, and Smooth Muscle Contraction in Human Prostate Tissues

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Xiaolong Wang ◽  
Yiming Wang ◽  
Christian Gratzke ◽  
Christian Sterr ◽  
Qingfeng Yu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Benign Prostatic Hyperplasia ◽  
Muscle Contraction ◽  
Stromal Cell ◽  
Molecular Mechanisms ◽  
Smooth Muscle Contraction ◽  
Prostatic Hyperplasia ◽  
Human Prostate ◽  
Mrna Levels ◽  
Prostate Enlargement

Epidemiologic studies revealed a context between lower urinary tract symptoms (LUTS) suggestive of benign prostatic hyperplasia (BPH) and metabolic syndrome. However, molecular mechanisms underlying this relationship are largely unknown. Prostate enlargement and increased prostate smooth muscle tone are important factors in the pathophysiology of LUTS suggestive of BPH. In the present study, we studied effects of the metabolic hormone ghrelin on prostate enlargement in rats with experimentally induced BPH, growth of cultured stromal cells from human prostate (WPMY-1), and smooth muscle contraction of human prostate tissues. Ghrelin (20 nmol/kg daily, p.o., 2 weeks) increased prostate size in rats with testosterone-induced BPH. Microarray identified 114 ghrelin-upregulated genes (2-fold or more) in these prostates, with possible roles in growth, smooth muscle contraction, or metabolism. 12 genes were selected for further analyses. In human prostate tissues, mRNA levels of 11 of them correlated positively with ghrelin receptor (GHSR) expression, but only two with the degree of BPH. Accordingly, no correlation was evident between GHSR expression level and BPH in human prostate tissues. In WPMY-1 cells, the GHRS agonist MK0677 upregulated 11 of the selected genes. MK0677 induced proliferation of WPMY-1 cells, shown by EdU assay, colony formation, proliferation markers, flow cytometry, and viability. In myographic measurements, GHSR agonists enhanced contractions of human prostate strips. Together, ghrelin may aggravate prostate enlargement, stromal cell growth, and prostate smooth muscle contraction in BPH. Ghrelin may deteriorate urethral obstruction independently from BPH, qualifying the ghrelin system as an attractive new target to be tested for LUTS treatment in BPH.

scholarly journals Benign prostatic hyperplasia treatment using plasmonic nanoparticles irradiated by laser in a rat model

2020 ◽  
Vol 127 ◽  
pp. 110118
Author(s):  
Omid Koohi Hosseinabadi ◽  
Mohammad Ali Behnam ◽  
Arezoo Khoradmehr ◽  
Farzin Emami ◽  
Zahra Sobhani ◽  
...  
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Rat Model ◽  
Prostatic Hyperplasia ◽  
Plasmonic Nanoparticles
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