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Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells
AIM: To investigate the effects of combined use of emodin and baicalein (CEB) at the cellular and organism levels in severe acute pancreatitis (SAP) and explore the underlying mechanism. METHODS: SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in 48 male SD...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5757123/ https://www.ncbi.nlm.nih.gov/pubmed/29358880 http://dx.doi.org/10.3748/wjg.v24.i1.35 |
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author | Li, Jun Zhou, Rui Bie, Bei-Bei Huang, Na Guo, Ying Chen, Hai-Yan Shi, Meng-Jiao Yang, Jun Zhang, Jian Li, Zong-Fang |
author_facet | Li, Jun Zhou, Rui Bie, Bei-Bei Huang, Na Guo, Ying Chen, Hai-Yan Shi, Meng-Jiao Yang, Jun Zhang, Jian Li, Zong-Fang |
author_sort | Li, Jun |
collection | PubMed |
description | AIM: To investigate the effects of combined use of emodin and baicalein (CEB) at the cellular and organism levels in severe acute pancreatitis (SAP) and explore the underlying mechanism. METHODS: SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in 48 male SD rats. Pancreatic histopathology score, serum amylase activity, and levels of tumour necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and IL-10 were determined to assess the effects of CEB at 12 h after the surgery. The rat pancreatic acinar cells were isolated from healthy male SD rats using collagenase. The cell viability, cell ultrastructure, intracellular free Ca(2+) concentration, and inositol (1,4,5)-trisphosphate receptor (IP(3)R) expression were investigated to assess the mechanism of CEB. RESULTS: Pancreatic histopathology score (2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05) and serum amylase activity (2866.2 ± 617.7 vs 5241.3 ± 1410.0, P < 0.05) were significantly decreased in the CEB (three doses) treatment group compared with the SAP group (2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05). CEB dose-dependently reduced the levels of the pro-inflammatory cytokines IL-6 (466.82 ± 48.55 vs 603.50 ± 75.53, P < 0.05) and TNF-α (108.04 ± 16.10 vs 215.56 ± 74.67, P < 0.05) and increased the level of the anti-inflammatory cytokine IL-10 (200.96 ± 50.76 vs 54.18 ± 6.07, P < 0.05) compared with those in the SAP group. CEB increased cell viability, inhibited cytosolic Ca(2+) concentration, and significantly ameliorated intracellular vacuoles and IP(3) mRNA expression compared with those in the SAP group (P < 0.05). There was a trend towards decreased IP(3)R protein in the CEB treatment group; however, it did not reach statistical significance (P > 0.05). CONCLUSION: These results at the cellular and organism levels reflect a preliminary mechanism of CEB in SAP and indicate that CEB is a suitable approach for SAP treatment. |
format | Online Article Text |
id | pubmed-5757123 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-57571232018-01-22 Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells Li, Jun Zhou, Rui Bie, Bei-Bei Huang, Na Guo, Ying Chen, Hai-Yan Shi, Meng-Jiao Yang, Jun Zhang, Jian Li, Zong-Fang World J Gastroenterol Basic Study AIM: To investigate the effects of combined use of emodin and baicalein (CEB) at the cellular and organism levels in severe acute pancreatitis (SAP) and explore the underlying mechanism. METHODS: SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in 48 male SD rats. Pancreatic histopathology score, serum amylase activity, and levels of tumour necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and IL-10 were determined to assess the effects of CEB at 12 h after the surgery. The rat pancreatic acinar cells were isolated from healthy male SD rats using collagenase. The cell viability, cell ultrastructure, intracellular free Ca(2+) concentration, and inositol (1,4,5)-trisphosphate receptor (IP(3)R) expression were investigated to assess the mechanism of CEB. RESULTS: Pancreatic histopathology score (2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05) and serum amylase activity (2866.2 ± 617.7 vs 5241.3 ± 1410.0, P < 0.05) were significantly decreased in the CEB (three doses) treatment group compared with the SAP group (2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05). CEB dose-dependently reduced the levels of the pro-inflammatory cytokines IL-6 (466.82 ± 48.55 vs 603.50 ± 75.53, P < 0.05) and TNF-α (108.04 ± 16.10 vs 215.56 ± 74.67, P < 0.05) and increased the level of the anti-inflammatory cytokine IL-10 (200.96 ± 50.76 vs 54.18 ± 6.07, P < 0.05) compared with those in the SAP group. CEB increased cell viability, inhibited cytosolic Ca(2+) concentration, and significantly ameliorated intracellular vacuoles and IP(3) mRNA expression compared with those in the SAP group (P < 0.05). There was a trend towards decreased IP(3)R protein in the CEB treatment group; however, it did not reach statistical significance (P > 0.05). CONCLUSION: These results at the cellular and organism levels reflect a preliminary mechanism of CEB in SAP and indicate that CEB is a suitable approach for SAP treatment. Baishideng Publishing Group Inc 2018-01-07 2018-01-07 /pmc/articles/PMC5757123/ /pubmed/29358880 http://dx.doi.org/10.3748/wjg.v24.i1.35 Text en ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. |
spellingShingle | Basic Study Li, Jun Zhou, Rui Bie, Bei-Bei Huang, Na Guo, Ying Chen, Hai-Yan Shi, Meng-Jiao Yang, Jun Zhang, Jian Li, Zong-Fang Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells |
title | Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells |
title_full | Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells |
title_fullStr | Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells |
title_full_unstemmed | Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells |
title_short | Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells |
title_sort | emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells |
topic | Basic Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5757123/ https://www.ncbi.nlm.nih.gov/pubmed/29358880 http://dx.doi.org/10.3748/wjg.v24.i1.35 |
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