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...
Main Authors: | , , , , , , , , , |
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Format: | Article |
Language: | English |
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Taylor & Francis Group
2021-01-01
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Series: | Pharmaceutical Biology |
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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. |
first_indexed | 2024-12-19T02:10:04Z |
format | Article |
id | doaj.art-d2b12f7d46c44782ac825165082e8b0c |
institution | Directory Open Access Journal |
issn | 1388-0209 1744-5116 |
language | English |
last_indexed | 2024-12-19T02:10:04Z |
publishDate | 2021-01-01 |
publisher | Taylor & Francis Group |
record_format | Article |
series | Pharmaceutical Biology |
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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