| Autor: |
Youn DH; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea., Park J; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea., Kim HL; College of Korean Medicine, Basic Research Laboratory for Comorbidity Regulation, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea., Jung Y; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea., Kang J; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea., Jeong MY; College of Korean Medicine, Basic Research Laboratory for Comorbidity Regulation, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea., Sethi G; Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, 117600, Singapore., Seok Ahn K; College of Korean Medicine, Basic Research Laboratory for Comorbidity Regulation, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea., Um JY; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea.; College of Korean Medicine, Basic Research Laboratory for Comorbidity Regulation, Kyung Hee University, Dongdaemun-Gu, Seoul, 02447, Republic of Korea. |
| Abstrakt: |
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. |
