Chrysophanic acid reduces testosterone-induced benign prostatic hyperplasia in rats by suppressing 5α-reductase and extracellular signal-regulated kinase
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Dong-Hyun Youn1,*, Jinbong Park1,*, Hye-Lin Kim2, Yunu Jung1, JongWook Kang1, Mi-Young Jeong2, Gautam Sethi3, Kwang Seok Ahn2, Jae-Young Um1,2
1Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea
2College of Korean Medicine, Basic Research Laboratory for Comorbidity Regulation, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea
3Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, 117600, Singapore
*These authors have contributed equally to this work
Jae-Young Um, email: email@example.com
Keywords: benign prostatic hyperplasia-BPH, chrysophanic acid, prostate specific antigen, 5α-reductase, extracellular signal-regulated kinase
Received: April 28, 2016 Accepted: October 31, 2016 Published: November 17, 2016
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, 5α-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 α 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.
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