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Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats

AIM: To investigate the mechanisms by which Sheng-jiang powder (SJP) ameliorates obesity-induced pancreatic inflammatory injury. METHODS: Sprague-Dawley rats were randomized into three groups: normal group (NG), obese group (HLG), or SJP treatment group (HSG). Obesity was induced by feeding a high-f...

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Autores principales: Miao, Yi-Fan, Li, Juan, Zhang, Yu-Mei, Zhu, Lv, Chen, Huan, Yuan, Ling, Hu, Jing, Yi, Xiao-Lin, Wu, Qiu-Ting, Wan, Mei-Hua, Tang, Wen-Fu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6196332/
https://www.ncbi.nlm.nih.gov/pubmed/30356974
http://dx.doi.org/10.3748/wjg.v24.i39.4448
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author Miao, Yi-Fan
Li, Juan
Zhang, Yu-Mei
Zhu, Lv
Chen, Huan
Yuan, Ling
Hu, Jing
Yi, Xiao-Lin
Wu, Qiu-Ting
Wan, Mei-Hua
Tang, Wen-Fu
author_facet Miao, Yi-Fan
Li, Juan
Zhang, Yu-Mei
Zhu, Lv
Chen, Huan
Yuan, Ling
Hu, Jing
Yi, Xiao-Lin
Wu, Qiu-Ting
Wan, Mei-Hua
Tang, Wen-Fu
author_sort Miao, Yi-Fan
collection PubMed
description AIM: To investigate the mechanisms by which Sheng-jiang powder (SJP) ameliorates obesity-induced pancreatic inflammatory injury. METHODS: Sprague-Dawley rats were randomized into three groups: normal group (NG), obese group (HLG), or SJP treatment group (HSG). Obesity was induced by feeding a high-fat diet in the HLG and HSG, while the NG received standard chow. Rats were euthanized after 12 wk, and blood and pancreatic tissues were collected for histopathological analyses. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and transforming growth factor beta (TGF-β) expression, serum triglyceride and adiponectin levels, and apoptosis in pancreatic acinar cells were assessed. A high-fat AR42J acinar cell injury model was established using very low-density lipoprotein (VLDL). AR42J acinar cell culture supernatant, treated with different interventions, was applied to seven groups of pancreatic stellate cells (PSCs). The proliferation of PSCs and the expression of fibronectin and type I collagenase were assessed. RESULTS: Compared with the NG, we found higher pathological scores for pancreatic tissues, lower serum adiponectin levels, higher expression levels of NF-κB in pancreatic tissues and TGF-β in pancreatic inflammatory cells, and increased apoptosis among pancreatic acinar cells for the HLG (P < 0.05). Compared with the HLG, we found reduced body weight, Lee’s index scores, serum triglyceride levels, and pathological scores for pancreatic tissues; higher serum adiponectin levels; and lower expression levels of NF-κB, in pancreatic tissue and TGF-β in pancreatic inflammatory cells for the HSG (P < 0.05). The in vitro studies showed enhanced PSC activation and increased expression levels of fibronectin and type I collagenase after SJP treatment. An adenosine 5‘-monophosphate-activated protein kinase (AMPK) inhibitor inhibited PSC activation. CONCLUSION: SJP may ameliorate obesity-induced pancreatic inflammatory injury in rats by regulating key molecules of the adiponectin-AMPK signalling pathway.
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spelling pubmed-61963322018-10-23 Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats Miao, Yi-Fan Li, Juan Zhang, Yu-Mei Zhu, Lv Chen, Huan Yuan, Ling Hu, Jing Yi, Xiao-Lin Wu, Qiu-Ting Wan, Mei-Hua Tang, Wen-Fu World J Gastroenterol Basic Study AIM: To investigate the mechanisms by which Sheng-jiang powder (SJP) ameliorates obesity-induced pancreatic inflammatory injury. METHODS: Sprague-Dawley rats were randomized into three groups: normal group (NG), obese group (HLG), or SJP treatment group (HSG). Obesity was induced by feeding a high-fat diet in the HLG and HSG, while the NG received standard chow. Rats were euthanized after 12 wk, and blood and pancreatic tissues were collected for histopathological analyses. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and transforming growth factor beta (TGF-β) expression, serum triglyceride and adiponectin levels, and apoptosis in pancreatic acinar cells were assessed. A high-fat AR42J acinar cell injury model was established using very low-density lipoprotein (VLDL). AR42J acinar cell culture supernatant, treated with different interventions, was applied to seven groups of pancreatic stellate cells (PSCs). The proliferation of PSCs and the expression of fibronectin and type I collagenase were assessed. RESULTS: Compared with the NG, we found higher pathological scores for pancreatic tissues, lower serum adiponectin levels, higher expression levels of NF-κB in pancreatic tissues and TGF-β in pancreatic inflammatory cells, and increased apoptosis among pancreatic acinar cells for the HLG (P < 0.05). Compared with the HLG, we found reduced body weight, Lee’s index scores, serum triglyceride levels, and pathological scores for pancreatic tissues; higher serum adiponectin levels; and lower expression levels of NF-κB, in pancreatic tissue and TGF-β in pancreatic inflammatory cells for the HSG (P < 0.05). The in vitro studies showed enhanced PSC activation and increased expression levels of fibronectin and type I collagenase after SJP treatment. An adenosine 5‘-monophosphate-activated protein kinase (AMPK) inhibitor inhibited PSC activation. CONCLUSION: SJP may ameliorate obesity-induced pancreatic inflammatory injury in rats by regulating key molecules of the adiponectin-AMPK signalling pathway. Baishideng Publishing Group Inc 2018-10-21 2018-10-21 /pmc/articles/PMC6196332/ /pubmed/30356974 http://dx.doi.org/10.3748/wjg.v24.i39.4448 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
Miao, Yi-Fan
Li, Juan
Zhang, Yu-Mei
Zhu, Lv
Chen, Huan
Yuan, Ling
Hu, Jing
Yi, Xiao-Lin
Wu, Qiu-Ting
Wan, Mei-Hua
Tang, Wen-Fu
Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats
title Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats
title_full Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats
title_fullStr Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats
title_full_unstemmed Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats
title_short Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats
title_sort sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the ampk signalling pathway in rats
topic Basic Study
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6196332/
https://www.ncbi.nlm.nih.gov/pubmed/30356974
http://dx.doi.org/10.3748/wjg.v24.i39.4448
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