Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.13430
Title: Chrysophanic acid reduces testosterone-induced benign prostatic hyperplasia in rats by suppressing 5?-reductase and extracellular signal-regulated kinase
Authors: Youn, D.-H
Park, J
Kim, H.-L
Jung, Y
Kang, J
Jeong, M.-Y
Sethi, G 
Ahn, K.S
Um, J.-Y
Keywords: androgen receptor
chrysophanic acid
estrogen receptor alpha
finasteride
mitogen activated protein kinase
mitogen activated protein kinase p38
prostate specific antigen
steroid 5alpha reductase
steroid receptor coactivator 1
stress activated protein kinase
testosterone propionate
animal experiment
animal model
animal tissue
antigen expression
antiproliferative activity
Article
cell proliferation
controlled study
down regulation
drug effect
enzyme inhibition
enzyme repression
histology
human
human cell
in vitro study
male
nonhuman
prostate epithelium cell
prostate hypertrophy
prostate weight
protein expression
rat
upregulation
Issue Date: 2017
Publisher: Impact Journals LLC
Citation: Youn, D.-H, Park, J, Kim, H.-L, Jung, Y, Kang, J, Jeong, M.-Y, Sethi, G, Ahn, K.S, Um, J.-Y (2017). Chrysophanic acid reduces testosterone-induced benign prostatic hyperplasia in rats by suppressing 5?-reductase and extracellular signal-regulated kinase. Oncotarget 8 (6) : 9500-9512. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.13430
Rights: Attribution 4.0 International
Abstract: Benign prostatic hyperplasia (BPH) is one of the most common chronic diseases in male population, of which incidence increases gradually with age. In this study, we investigated the effect of chrysophanic acid (CA) on BPH. BPH was induced by a 4-week injection of testosterone propionate (TP). Four weeks of further injection with vehicle, TP, TP + CA, TP + finasteride was carried on. In the CA treatment group, the prostate weight was reduced and the TP-induced histological changes were restored as the normal control group. CA treatment suppressed the TP-elevated prostate specific antigen (PSA) expression. In addition, 5?-reductase, a crucial factor in BPH development, was suppressed to the normal level close to the control group by CA treatment. The elevated expressions of androgen receptor (AR), estrogen receptor a and steroid receptor coactivator 1 by TP administration were also inhibited in the CA group when compared to the TP-induced BPH group. Then we evaluated the changes in three major factors of the mitogen-activated protein kinase chain during prostatic hyperplasia; extracellular signal-regulated kinase (ERK), c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38). While ERK was elevated in the process of BPH, JNK and p38 was not changed. This up-regulated ERK was also reduced as normal by CA treatment. Further in vitro studies with RWPE-1 cells confirmed TP-induced proliferation and elevated AR, PSA and p-ERK were all reduced by CA treatment. Overall, these results suggest a potential pharmaceutical feature of CA in the treatment of BPH.
Source Title: Oncotarget
URI: https://scholarbank.nus.edu.sg/handle/10635/179769
ISSN: 1949-2553
DOI: 10.18632/oncotarget.13430
Rights: Attribution 4.0 International
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