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Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca(2+) related regulators

BACKGROUND AND AIM: Panax ginseng, a key herbal medicine of replenishing Qi and tonifying Spleen, is widely used in the treatment of gastrointestinal diseases in East Asia. In this study, we aim to investigate the potential effects and mechanisms of polysaccharides from P. ginseng (PGP) on intestina...

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Autores principales: Zhu, Huibin, Cao, Jianhong, Liang, Xinyi, Luo, Meng, Wang, Anrong, Hu, Ling, Li, Ruliu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9834020/
https://www.ncbi.nlm.nih.gov/pubmed/36644379
http://dx.doi.org/10.1016/j.jgr.2022.05.010
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author Zhu, Huibin
Cao, Jianhong
Liang, Xinyi
Luo, Meng
Wang, Anrong
Hu, Ling
Li, Ruliu
author_facet Zhu, Huibin
Cao, Jianhong
Liang, Xinyi
Luo, Meng
Wang, Anrong
Hu, Ling
Li, Ruliu
author_sort Zhu, Huibin
collection PubMed
description BACKGROUND AND AIM: Panax ginseng, a key herbal medicine of replenishing Qi and tonifying Spleen, is widely used in the treatment of gastrointestinal diseases in East Asia. In this study, we aim to investigate the potential effects and mechanisms of polysaccharides from P. ginseng (PGP) on intestinal mucosal restitution which is one of the crucial repair modalities during the recovery of mucosal injury controlled by the Ca(2+) signaling. METHODS: Rat model of intestinal mucosal injury was induced by indomethacin. The fractional cell migration was carried out by immunohistochemistry staining with BrdU. The morphological observations on intestinal mucosal injury were also performed. Intestinal epithelial cell (IEC-6) migration in vitro was conducted by scratch method. Western-blot was adopted to determine the expressions of PLC-γ1, Rac1, TRPC1, RhoA and Cav-1. Immunoprecipitation was used to evaluate the levels of Rac1/PLC-γ1, RhoA/TRPC1 and Cav-1/TRPC1. RESULTS: The results showed that PGP effectively reduced the assessment of intestinal mucosal injury, reversed the inhibition of epithelial cell migration induced by Indomethacin, and increased the level of Ca(2+) in intestinal mucosa in vivo. Moreover, PGP dramatically promoted IEC-6 cell migration, the expression of Ca(2+) regulators (PLC-γ1, Rac1, TRPC1, Cav-1 and RhoA) as well as protein complexes (Rac1/PLC-γ1, Cav-1/TRPC1 and RhoA/TRPC1) in vitro. CONCLUSION: PGP increases the Ca(2+) content in intestinal mucosa partly through controlling the regulators of Ca(2+) mobilization, subsequently promotes intestinal epithelial cell migration, and then prevents intestinal mucosal injury induced by indomethacin.
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spelling pubmed-98340202023-01-13 Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca(2+) related regulators Zhu, Huibin Cao, Jianhong Liang, Xinyi Luo, Meng Wang, Anrong Hu, Ling Li, Ruliu J Ginseng Res Research Article BACKGROUND AND AIM: Panax ginseng, a key herbal medicine of replenishing Qi and tonifying Spleen, is widely used in the treatment of gastrointestinal diseases in East Asia. In this study, we aim to investigate the potential effects and mechanisms of polysaccharides from P. ginseng (PGP) on intestinal mucosal restitution which is one of the crucial repair modalities during the recovery of mucosal injury controlled by the Ca(2+) signaling. METHODS: Rat model of intestinal mucosal injury was induced by indomethacin. The fractional cell migration was carried out by immunohistochemistry staining with BrdU. The morphological observations on intestinal mucosal injury were also performed. Intestinal epithelial cell (IEC-6) migration in vitro was conducted by scratch method. Western-blot was adopted to determine the expressions of PLC-γ1, Rac1, TRPC1, RhoA and Cav-1. Immunoprecipitation was used to evaluate the levels of Rac1/PLC-γ1, RhoA/TRPC1 and Cav-1/TRPC1. RESULTS: The results showed that PGP effectively reduced the assessment of intestinal mucosal injury, reversed the inhibition of epithelial cell migration induced by Indomethacin, and increased the level of Ca(2+) in intestinal mucosa in vivo. Moreover, PGP dramatically promoted IEC-6 cell migration, the expression of Ca(2+) regulators (PLC-γ1, Rac1, TRPC1, Cav-1 and RhoA) as well as protein complexes (Rac1/PLC-γ1, Cav-1/TRPC1 and RhoA/TRPC1) in vitro. CONCLUSION: PGP increases the Ca(2+) content in intestinal mucosa partly through controlling the regulators of Ca(2+) mobilization, subsequently promotes intestinal epithelial cell migration, and then prevents intestinal mucosal injury induced by indomethacin. Elsevier 2023-01 2022-05-27 /pmc/articles/PMC9834020/ /pubmed/36644379 http://dx.doi.org/10.1016/j.jgr.2022.05.010 Text en © 2022 The Korean Society of Ginseng. Publishing services by Elsevier B.V. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Article
Zhu, Huibin
Cao, Jianhong
Liang, Xinyi
Luo, Meng
Wang, Anrong
Hu, Ling
Li, Ruliu
Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca(2+) related regulators
title Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca(2+) related regulators
title_full Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca(2+) related regulators
title_fullStr Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca(2+) related regulators
title_full_unstemmed Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca(2+) related regulators
title_short Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca(2+) related regulators
title_sort polysaccharides from panax ginseng promote intestinal epithelial cell migration through affecting the ca(2+) related regulators
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9834020/
https://www.ncbi.nlm.nih.gov/pubmed/36644379
http://dx.doi.org/10.1016/j.jgr.2022.05.010
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