Cargando…

Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway

PURPOSE: Nonalcoholic fatty liver disease (NAFLD) has become a predictor of death in many diseases. This study was carried out to investigate the therapeutic effect of Radix Polygoni Multiflori Preparata (RPMP) and its main component emodin on egg yolk powder-induced NAFLD in zebrafish. Further inve...

Descripción completa

Detalles Bibliográficos
Autores principales: Yu, Linyuan, Gong, Lihong, Wang, Cheng, Hu, Naihua, Tang, Yunqiu, Zheng, Li, Dai, Xuyang, Li, Yunxia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167271/
https://www.ncbi.nlm.nih.gov/pubmed/32346285
http://dx.doi.org/10.2147/DDDT.S243893
_version_ 1783523549704617984
author Yu, Linyuan
Gong, Lihong
Wang, Cheng
Hu, Naihua
Tang, Yunqiu
Zheng, Li
Dai, Xuyang
Li, Yunxia
author_facet Yu, Linyuan
Gong, Lihong
Wang, Cheng
Hu, Naihua
Tang, Yunqiu
Zheng, Li
Dai, Xuyang
Li, Yunxia
author_sort Yu, Linyuan
collection PubMed
description PURPOSE: Nonalcoholic fatty liver disease (NAFLD) has become a predictor of death in many diseases. This study was carried out to investigate the therapeutic effect of Radix Polygoni Multiflori Preparata (RPMP) and its main component emodin on egg yolk powder-induced NAFLD in zebrafish. Further investigation was performed to explore whether emodin was the main component of RPMP for the treatment of NAFLD as well as the underlying therapeutic mechanism of RPMP and emodin. METHODS: Zebrafish were divided into control group, egg yolk powder group, RPMP group and emodin group. The obesity of zebrafish was evaluated by body weight, body length and BMI. The content of lipid was detected by triglyceride (TG), total cholesterol (TC) reagent kit and the fatty acid was detected by nonesterified free fatty acids (NEFA) reagent kit. HE staining was used to detect the histological structure of liver. Whole-mount Oil red O staining and Frozen oil red O staining were carried out to investigate the lipid accumulation in liver. KEGG and STRING databases were performed to analyze the potential role of AMPK between insulin resistance (IR) and fatty acid oxidation. Western blot and RT-qPCR were carried out for mechanism research. RESULTS: RPMP and emodin significantly reduced zebrafish weight, body length and BMI. Both RPMP and emodin treatment could reduce the lipid deposition in zebrafish liver. RPMP significantly reduced the content of TG. However, emodin significantly reduced the contents of TG, TC and NEFA in zebrafish with NAFLD. The protein interaction network indicated that AMPK participated in both IR and fatty acid oxidation. Further investigation indicated that RPMP and emodin reduced hepatic lipogenesis via up-regulating the expressions of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT2), amp-activated protein kinase alpha (AMPKα), proliferator-activated receptor alpha (PPARα), carnitine palmitoyl transferase 1a (CPT-1a) and acyl-coenzyme A oxidase 1 (ACOX1). CONCLUSION: These findings suggest that emodin is the main component of RPMP for the treatment of NAFLD, which is closely related to the regulation of AMPK signaling pathway which increases IR and fatty acid oxidation.
format Online
Article
Text
id pubmed-7167271
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher Dove
record_format MEDLINE/PubMed
spelling pubmed-71672712020-04-28 Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway Yu, Linyuan Gong, Lihong Wang, Cheng Hu, Naihua Tang, Yunqiu Zheng, Li Dai, Xuyang Li, Yunxia Drug Des Devel Ther Original Research PURPOSE: Nonalcoholic fatty liver disease (NAFLD) has become a predictor of death in many diseases. This study was carried out to investigate the therapeutic effect of Radix Polygoni Multiflori Preparata (RPMP) and its main component emodin on egg yolk powder-induced NAFLD in zebrafish. Further investigation was performed to explore whether emodin was the main component of RPMP for the treatment of NAFLD as well as the underlying therapeutic mechanism of RPMP and emodin. METHODS: Zebrafish were divided into control group, egg yolk powder group, RPMP group and emodin group. The obesity of zebrafish was evaluated by body weight, body length and BMI. The content of lipid was detected by triglyceride (TG), total cholesterol (TC) reagent kit and the fatty acid was detected by nonesterified free fatty acids (NEFA) reagent kit. HE staining was used to detect the histological structure of liver. Whole-mount Oil red O staining and Frozen oil red O staining were carried out to investigate the lipid accumulation in liver. KEGG and STRING databases were performed to analyze the potential role of AMPK between insulin resistance (IR) and fatty acid oxidation. Western blot and RT-qPCR were carried out for mechanism research. RESULTS: RPMP and emodin significantly reduced zebrafish weight, body length and BMI. Both RPMP and emodin treatment could reduce the lipid deposition in zebrafish liver. RPMP significantly reduced the content of TG. However, emodin significantly reduced the contents of TG, TC and NEFA in zebrafish with NAFLD. The protein interaction network indicated that AMPK participated in both IR and fatty acid oxidation. Further investigation indicated that RPMP and emodin reduced hepatic lipogenesis via up-regulating the expressions of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT2), amp-activated protein kinase alpha (AMPKα), proliferator-activated receptor alpha (PPARα), carnitine palmitoyl transferase 1a (CPT-1a) and acyl-coenzyme A oxidase 1 (ACOX1). CONCLUSION: These findings suggest that emodin is the main component of RPMP for the treatment of NAFLD, which is closely related to the regulation of AMPK signaling pathway which increases IR and fatty acid oxidation. Dove 2020-04-15 /pmc/articles/PMC7167271/ /pubmed/32346285 http://dx.doi.org/10.2147/DDDT.S243893 Text en © 2020 Yu et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Yu, Linyuan
Gong, Lihong
Wang, Cheng
Hu, Naihua
Tang, Yunqiu
Zheng, Li
Dai, Xuyang
Li, Yunxia
Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway
title Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway
title_full Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway
title_fullStr Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway
title_full_unstemmed Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway
title_short Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway
title_sort radix polygoni multiflori and its main component emodin attenuate non-alcoholic fatty liver disease in zebrafish by regulation of ampk signaling pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167271/
https://www.ncbi.nlm.nih.gov/pubmed/32346285
http://dx.doi.org/10.2147/DDDT.S243893
work_keys_str_mv AT yulinyuan radixpolygonimultiflorianditsmaincomponentemodinattenuatenonalcoholicfattyliverdiseaseinzebrafishbyregulationofampksignalingpathway
AT gonglihong radixpolygonimultiflorianditsmaincomponentemodinattenuatenonalcoholicfattyliverdiseaseinzebrafishbyregulationofampksignalingpathway
AT wangcheng radixpolygonimultiflorianditsmaincomponentemodinattenuatenonalcoholicfattyliverdiseaseinzebrafishbyregulationofampksignalingpathway
AT hunaihua radixpolygonimultiflorianditsmaincomponentemodinattenuatenonalcoholicfattyliverdiseaseinzebrafishbyregulationofampksignalingpathway
AT tangyunqiu radixpolygonimultiflorianditsmaincomponentemodinattenuatenonalcoholicfattyliverdiseaseinzebrafishbyregulationofampksignalingpathway
AT zhengli radixpolygonimultiflorianditsmaincomponentemodinattenuatenonalcoholicfattyliverdiseaseinzebrafishbyregulationofampksignalingpathway
AT daixuyang radixpolygonimultiflorianditsmaincomponentemodinattenuatenonalcoholicfattyliverdiseaseinzebrafishbyregulationofampksignalingpathway
AT liyunxia radixpolygonimultiflorianditsmaincomponentemodinattenuatenonalcoholicfattyliverdiseaseinzebrafishbyregulationofampksignalingpathway