ArticleOncotarget2017
Chrysophanic acid reduces testosterone-induced benign prostatic hyperplasia in rats by suppressing 5α-reductase and extracellular signal-regulated kinase.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Curcumin targets miR-21-3p: promising therapeutic strategy for treatment of benign prostatic hyperplasia.Molecular biology reports · 2025Article
- Portulaca oleracea Extract Ameliorates Testosterone Propionate-Induced Benign Prostatic Hyperplasia in Male Sprague-Dawley Rats.Veterinary medicine and science · 2025Article
- Heat-Killed and LiveJournal of microbiology and biotechnology · 2021Article
- Umbelliferone Ameliorates Benign Prostatic Hyperplasia by Inhibiting Cell Proliferation and G1/S Phase Cell Cycle Progression through Regulation of STAT3/E2F1 Axis.International journal of molecular sciences · 2021Article
- Molecular mechanisms and associated cell signalling pathways underlying the anticancer properties of phytochemical compounds fromExperimental and therapeutic medicine · 2021Review
- Phytosterols in hull-less pumpkin seed oil, rich in ∆Food & nutrition research · 2021Article
- Tight junction protein claudin-1 is downregulated by TGF-β1 via MEK signaling in benign prostatic epithelial cells.The Prostate · 2020Article
- Immunomodulatory effect of diallyl sulfide on experimentally-induced benign prostate hyperplasia via the suppression of CD4+T/IL-17 and TGF-β1/ERK pathways.Inflammopharmacology · 2020Article
- Transforming growth factor beta 1 impairs benign prostatic luminal epithelial cell monolayer barrier function.American journal of clinical and experimental urology · 2020Article
- Resveratrol induces apoptosis of benign prostatic hyperplasia epithelial cell line (BPH-1) through p38 MAPK-FOXO3a pathway.BMC complementary and alternative medicine · 2019Article
- Taeumjowi-tang, a Traditional Korean Sasang Remedy, Improves Obesity-Atopic Dermatitis Comorbidity by Regulating Hypoxia-Inducible Factor 1 Alpha.Frontiers in pharmacology · 2019Article
- Aconiti Lateralis Radix Preparata, the Dried Root ofEvidence-based complementary and alternative medicine : eCAM · 2019Article
- Specific expression pattern of tissue cytokines analyzed through the Surface Acoustic Wave technique is associated with age-related spontaneous benign prostatic hyperplasia in rats.Biochemistry and biophysics reports · 2018Article
- Berberine Improves Benign Prostatic Hyperplasia via Suppression of 5 Alpha Reductase and Extracellular Signal-Regulated KinaseFrontiers in pharmacology · 2018Article
- Artemether suppresses cell proliferation and induces apoptosis in diffuse large B cell lymphoma cells.Experimental and therapeutic medicine · 2017Article
- Vanillic acid attenuates testosterone-induced benign prostatic hyperplasia in rats and inhibits proliferation of prostatic epithelial cells.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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, 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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