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Loureirin B inhibits the proliferation of hepatic stellate cells and the Wnt/β-catenin signaling pathway by regulating miR-148-3p

BACKGROUND: We investigated the activity of loureirin B against liver fibrosis and the underlying molecular mechanisms. METHODS: Hepatic stellate cells (HSCs) from Sprague-Dawley rats were treated with different concentrations of loureirin B. We used the MTT assay to determine HSC proliferation, flo...

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Autores principales: Hu, Jian-Peng, Zhang, Rong, Tang, Min, Li, Yu-Lian, Xun, Lin-Ting, Shi, Zhi-Zhou, An, Ying, Li, Ting, Song, Zheng-Ji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090993/
https://www.ncbi.nlm.nih.gov/pubmed/30123297
http://dx.doi.org/10.1186/s11658-018-0098-9
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author Hu, Jian-Peng
Zhang, Rong
Tang, Min
Li, Yu-Lian
Xun, Lin-Ting
Shi, Zhi-Zhou
An, Ying
Li, Ting
Song, Zheng-Ji
author_facet Hu, Jian-Peng
Zhang, Rong
Tang, Min
Li, Yu-Lian
Xun, Lin-Ting
Shi, Zhi-Zhou
An, Ying
Li, Ting
Song, Zheng-Ji
author_sort Hu, Jian-Peng
collection PubMed
description BACKGROUND: We investigated the activity of loureirin B against liver fibrosis and the underlying molecular mechanisms. METHODS: Hepatic stellate cells (HSCs) from Sprague-Dawley rats were treated with different concentrations of loureirin B. We used the MTT assay to determine HSC proliferation, flow cytometry to analyze apoptosis, and western blot to determine the expressions of Bax, Bcl-2, Wnt1 and β-catenin. Real-time PCR was used to determine the expressions of Wnt1 and miR-148-3p. RESULTS: The MTT assay showed that loureirin B treatment significantly inhibited the proliferation of HSCs in time- and dose-dependent manners. Loureirin B significantly promoted the apoptosis of HSCs, increased the expression of Bax and decreased the Bcl-2 level. Western blot analysis showed that the expressions of Wnt1 and β-catenin were obviously lower in the loureirin B treatment group than in the control group. We also found that loureirin B could decrease the Wnt1 mRNA level and increase miR-148-3p expression. Knockdown of miR-148-3p using inhibitor could reverse the effects of loureirin B on the proliferation and apoptosis of HSCs and the expressions of Bax, Bcl-2, Wnt1 and β-catenin. CONCLUSION: Our results suggest that loureirin B inhibited the proliferation and promoted the apoptosis of HSCs, and suppressed the Wnt/β-catenin signaling pathway via regulation of miR-148-3p.
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spelling pubmed-60909932018-08-17 Loureirin B inhibits the proliferation of hepatic stellate cells and the Wnt/β-catenin signaling pathway by regulating miR-148-3p Hu, Jian-Peng Zhang, Rong Tang, Min Li, Yu-Lian Xun, Lin-Ting Shi, Zhi-Zhou An, Ying Li, Ting Song, Zheng-Ji Cell Mol Biol Lett Research BACKGROUND: We investigated the activity of loureirin B against liver fibrosis and the underlying molecular mechanisms. METHODS: Hepatic stellate cells (HSCs) from Sprague-Dawley rats were treated with different concentrations of loureirin B. We used the MTT assay to determine HSC proliferation, flow cytometry to analyze apoptosis, and western blot to determine the expressions of Bax, Bcl-2, Wnt1 and β-catenin. Real-time PCR was used to determine the expressions of Wnt1 and miR-148-3p. RESULTS: The MTT assay showed that loureirin B treatment significantly inhibited the proliferation of HSCs in time- and dose-dependent manners. Loureirin B significantly promoted the apoptosis of HSCs, increased the expression of Bax and decreased the Bcl-2 level. Western blot analysis showed that the expressions of Wnt1 and β-catenin were obviously lower in the loureirin B treatment group than in the control group. We also found that loureirin B could decrease the Wnt1 mRNA level and increase miR-148-3p expression. Knockdown of miR-148-3p using inhibitor could reverse the effects of loureirin B on the proliferation and apoptosis of HSCs and the expressions of Bax, Bcl-2, Wnt1 and β-catenin. CONCLUSION: Our results suggest that loureirin B inhibited the proliferation and promoted the apoptosis of HSCs, and suppressed the Wnt/β-catenin signaling pathway via regulation of miR-148-3p. BioMed Central 2018-08-02 /pmc/articles/PMC6090993/ /pubmed/30123297 http://dx.doi.org/10.1186/s11658-018-0098-9 Text en © The Author(s) 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Hu, Jian-Peng
Zhang, Rong
Tang, Min
Li, Yu-Lian
Xun, Lin-Ting
Shi, Zhi-Zhou
An, Ying
Li, Ting
Song, Zheng-Ji
Loureirin B inhibits the proliferation of hepatic stellate cells and the Wnt/β-catenin signaling pathway by regulating miR-148-3p
title Loureirin B inhibits the proliferation of hepatic stellate cells and the Wnt/β-catenin signaling pathway by regulating miR-148-3p
title_full Loureirin B inhibits the proliferation of hepatic stellate cells and the Wnt/β-catenin signaling pathway by regulating miR-148-3p
title_fullStr Loureirin B inhibits the proliferation of hepatic stellate cells and the Wnt/β-catenin signaling pathway by regulating miR-148-3p
title_full_unstemmed Loureirin B inhibits the proliferation of hepatic stellate cells and the Wnt/β-catenin signaling pathway by regulating miR-148-3p
title_short Loureirin B inhibits the proliferation of hepatic stellate cells and the Wnt/β-catenin signaling pathway by regulating miR-148-3p
title_sort loureirin b inhibits the proliferation of hepatic stellate cells and the wnt/β-catenin signaling pathway by regulating mir-148-3p
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090993/
https://www.ncbi.nlm.nih.gov/pubmed/30123297
http://dx.doi.org/10.1186/s11658-018-0098-9
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