Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membrane-bound inhibitor

Context Inflammation and epithelial-mesenchymal transition (EMT) play important roles in the occurrence and development of benign prostatic hyperplasia (BPH); curcumin exerts anti-proliferative, anti-inflammatory, and anti-EMT effects. Objective To explore the anti-inflammatory and anti-EMT mechanis...

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Main Authors: Yuhang Liu, Zhaohui Wang, Yu Gan, Xiang Chen, Bo Zhang, Zhi Chen, Peihuan Liu, Bingsheng Li, Feng Ru, Yao He
Format: Article
Language:English
Published: Taylor & Francis Group 2021-01-01
Series:Pharmaceutical Biology
Subjects:
Online Access:http://dx.doi.org/10.1080/13880209.2021.1953539
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author Yuhang Liu
Zhaohui Wang
Yu Gan
Xiang Chen
Bo Zhang
Zhi Chen
Peihuan Liu
Bingsheng Li
Feng Ru
Yao He
author_facet Yuhang Liu
Zhaohui Wang
Yu Gan
Xiang Chen
Bo Zhang
Zhi Chen
Peihuan Liu
Bingsheng Li
Feng Ru
Yao He
author_sort Yuhang Liu
collection DOAJ
description Context Inflammation and epithelial-mesenchymal transition (EMT) play important roles in the occurrence and development of benign prostatic hyperplasia (BPH); curcumin exerts anti-proliferative, anti-inflammatory, and anti-EMT effects. Objective To explore the anti-inflammatory and anti-EMT mechanisms of curcumin in BPH. Materials and methods Ten-week-old male C57BL/6 mice were administered lipopolysaccharide (LPS, 100 µg/kg) in the prostate lobules to establish an inflammatory BPH model (LPS group), and curcumin (120 mg/kg) was administered into the abdominal cavity for 2 weeks (three times a week, curcumin-treated group). A group of healthy mice served as the control group. The expression of Toll-like receptor 4 (TLR4), bone morphogenetic protein and activin membrane-bound inhibitor (BAMBI), EMT markers, inflammatory cytokines, and transforming growth factor β1 (TGF-β1) was detected by PCR and western blotting. TGF-β1 (0.1 ng/mL) and LPS (100 ng/mL) were used to induce EMT in benign prostatic hyperplasia epithelial cells (BPH-1). Results In vivo, curcumin reduced the size of the prostate, suppressed the expression of vimentin and TLR4, and increased the expression of E-cadherin and BAMBI in the LPS-induced BPH mouse model. Moreover, curcumin decreased the levels of IL-6 and TNF-α by 44.52 and 46.17%, respectively. In vitro, curcumin attenuated cell proliferation, suppressed the expression of vimentin and TLR4, and increased the expression of E-cadherin and BAMBI in BPH-1 cells. Furthermore, BAMBI knockdown reversed the expression of vimentin and E-cadherin induced by curcumin. Discussion and conclusion This study demonstrated that curcumin alleviated hyperplasia, EMT, and inflammation in vivo. Furthermore, curcumin suppressed EMT by targeting BAMBI via the TLR4/BAMBI/TGF-β1 signalling pathway in vitro, demonstrating its potential utility in BPH treatment.
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spelling doaj.art-d2b12f7d46c44782ac825165082e8b0c2022-12-21T20:40:50ZengTaylor & Francis GroupPharmaceutical Biology1388-02091744-51162021-01-015911026103510.1080/13880209.2021.19535391953539Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membrane-bound inhibitorYuhang Liu0Zhaohui Wang1Yu Gan2Xiang Chen3Bo Zhang4Zhi Chen5Peihuan Liu6Bingsheng Li7Feng Ru8Yao He9Department of Urology, Hunan Children's HospitalDepartment of Urology, Hunan Children's HospitalDepartment of Urology, Xiangya Hospital, Central South UniversityDepartment of Urology, Xiangya Hospital, Central South UniversityDepartment of Urology, Xiangya Hospital, Central South UniversityDepartment of Urology, Xiangya Hospital, Central South UniversityDepartment of Urology, Xiangya Hospital, Central South UniversityDepartment of Urology, Xiangya Hospital, Central South UniversityDepartment of Urology, Xiangya Hospital, Central South UniversityDepartment of Urology, Xiangya Hospital, Central South UniversityContext Inflammation and epithelial-mesenchymal transition (EMT) play important roles in the occurrence and development of benign prostatic hyperplasia (BPH); curcumin exerts anti-proliferative, anti-inflammatory, and anti-EMT effects. Objective To explore the anti-inflammatory and anti-EMT mechanisms of curcumin in BPH. Materials and methods Ten-week-old male C57BL/6 mice were administered lipopolysaccharide (LPS, 100 µg/kg) in the prostate lobules to establish an inflammatory BPH model (LPS group), and curcumin (120 mg/kg) was administered into the abdominal cavity for 2 weeks (three times a week, curcumin-treated group). A group of healthy mice served as the control group. The expression of Toll-like receptor 4 (TLR4), bone morphogenetic protein and activin membrane-bound inhibitor (BAMBI), EMT markers, inflammatory cytokines, and transforming growth factor β1 (TGF-β1) was detected by PCR and western blotting. TGF-β1 (0.1 ng/mL) and LPS (100 ng/mL) were used to induce EMT in benign prostatic hyperplasia epithelial cells (BPH-1). Results In vivo, curcumin reduced the size of the prostate, suppressed the expression of vimentin and TLR4, and increased the expression of E-cadherin and BAMBI in the LPS-induced BPH mouse model. Moreover, curcumin decreased the levels of IL-6 and TNF-α by 44.52 and 46.17%, respectively. In vitro, curcumin attenuated cell proliferation, suppressed the expression of vimentin and TLR4, and increased the expression of E-cadherin and BAMBI in BPH-1 cells. Furthermore, BAMBI knockdown reversed the expression of vimentin and E-cadherin induced by curcumin. Discussion and conclusion This study demonstrated that curcumin alleviated hyperplasia, EMT, and inflammation in vivo. Furthermore, curcumin suppressed EMT by targeting BAMBI via the TLR4/BAMBI/TGF-β1 signalling pathway in vitro, demonstrating its potential utility in BPH treatment.http://dx.doi.org/10.1080/13880209.2021.1953539benign prostatic hyperplasiaepithelial-mesenchymal transitionlipopolysaccharidetoll-like receptor 4tumour necrosis factor-α
spellingShingle Yuhang Liu
Zhaohui Wang
Yu Gan
Xiang Chen
Bo Zhang
Zhi Chen
Peihuan Liu
Bingsheng Li
Feng Ru
Yao He
Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membrane-bound inhibitor
Pharmaceutical Biology
benign prostatic hyperplasia
epithelial-mesenchymal transition
lipopolysaccharide
toll-like receptor 4
tumour necrosis factor-α
title Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membrane-bound inhibitor
title_full Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membrane-bound inhibitor
title_fullStr Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membrane-bound inhibitor
title_full_unstemmed Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membrane-bound inhibitor
title_short Curcumin attenuates prostatic hyperplasia caused by inflammation via up-regulation of bone morphogenetic protein and activin membrane-bound inhibitor
title_sort curcumin attenuates prostatic hyperplasia caused by inflammation via up regulation of bone morphogenetic protein and activin membrane bound inhibitor
topic benign prostatic hyperplasia
epithelial-mesenchymal transition
lipopolysaccharide
toll-like receptor 4
tumour necrosis factor-α
url http://dx.doi.org/10.1080/13880209.2021.1953539
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