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Atractylodin Induces Myosin Light Chain Phosphorylation and Promotes Gastric Emptying through Ghrelin Receptor

Atractylodin is one of the main constituents in the rhizomes of Atractylodes lancea Thunb., being capable of treating cancer cachexia-anorexia and age-related diseases as an agonist of growth hormone secretagogue receptor (GHSR). GHSR was herein expressed in human gastric smooth muscle cells (HGSMCs...

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Autores principales: Bai, Yu, Zhao, Yan-hua, Xu, Jian-ya, Yu, Xi-zhong, Hu, Yun-xia, Zhao, Zhi-qiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572613/
https://www.ncbi.nlm.nih.gov/pubmed/28883883
http://dx.doi.org/10.1155/2017/2186798
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author Bai, Yu
Zhao, Yan-hua
Xu, Jian-ya
Yu, Xi-zhong
Hu, Yun-xia
Zhao, Zhi-qiang
author_facet Bai, Yu
Zhao, Yan-hua
Xu, Jian-ya
Yu, Xi-zhong
Hu, Yun-xia
Zhao, Zhi-qiang
author_sort Bai, Yu
collection PubMed
description Atractylodin is one of the main constituents in the rhizomes of Atractylodes lancea Thunb., being capable of treating cancer cachexia-anorexia and age-related diseases as an agonist of growth hormone secretagogue receptor (GHSR). GHSR was herein expressed in human gastric smooth muscle cells (HGSMCs) and activated by ghrelin receptor agonist L-692,585. Like L-692,585, atractylodin also increased Ca(2+) and enhanced the phosphorylation of myosin light chain (MLC) through GHSR in HGSMCs. In addition, atractylodin promoted gastric emptying and MLC phosphorylation in the gastric antrum of mice also through GHSR. Collectively, atractylodin can activate GHSR in gastric smooth muscle, as a potential target in clinical practice.
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spelling pubmed-55726132017-09-07 Atractylodin Induces Myosin Light Chain Phosphorylation and Promotes Gastric Emptying through Ghrelin Receptor Bai, Yu Zhao, Yan-hua Xu, Jian-ya Yu, Xi-zhong Hu, Yun-xia Zhao, Zhi-qiang Evid Based Complement Alternat Med Research Article Atractylodin is one of the main constituents in the rhizomes of Atractylodes lancea Thunb., being capable of treating cancer cachexia-anorexia and age-related diseases as an agonist of growth hormone secretagogue receptor (GHSR). GHSR was herein expressed in human gastric smooth muscle cells (HGSMCs) and activated by ghrelin receptor agonist L-692,585. Like L-692,585, atractylodin also increased Ca(2+) and enhanced the phosphorylation of myosin light chain (MLC) through GHSR in HGSMCs. In addition, atractylodin promoted gastric emptying and MLC phosphorylation in the gastric antrum of mice also through GHSR. Collectively, atractylodin can activate GHSR in gastric smooth muscle, as a potential target in clinical practice. Hindawi 2017 2017-08-13 /pmc/articles/PMC5572613/ /pubmed/28883883 http://dx.doi.org/10.1155/2017/2186798 Text en Copyright © 2017 Yu Bai et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Bai, Yu
Zhao, Yan-hua
Xu, Jian-ya
Yu, Xi-zhong
Hu, Yun-xia
Zhao, Zhi-qiang
Atractylodin Induces Myosin Light Chain Phosphorylation and Promotes Gastric Emptying through Ghrelin Receptor
title Atractylodin Induces Myosin Light Chain Phosphorylation and Promotes Gastric Emptying through Ghrelin Receptor
title_full Atractylodin Induces Myosin Light Chain Phosphorylation and Promotes Gastric Emptying through Ghrelin Receptor
title_fullStr Atractylodin Induces Myosin Light Chain Phosphorylation and Promotes Gastric Emptying through Ghrelin Receptor
title_full_unstemmed Atractylodin Induces Myosin Light Chain Phosphorylation and Promotes Gastric Emptying through Ghrelin Receptor
title_short Atractylodin Induces Myosin Light Chain Phosphorylation and Promotes Gastric Emptying through Ghrelin Receptor
title_sort atractylodin induces myosin light chain phosphorylation and promotes gastric emptying through ghrelin receptor
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572613/
https://www.ncbi.nlm.nih.gov/pubmed/28883883
http://dx.doi.org/10.1155/2017/2186798
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