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Butyric acid alleviated chronic intermittent hypoxia-induced lipid formation and inflammation through up-regulating HuR expression and inactivating AMPK pathways

To investigate whether butyric acid could alleviate chronic intermittent hypoxia (CIH)-induced lipid formation in human preadipocytes-subcutaneous (HPA-s) through accumulation of human antigen R (HuR) and inactivation of AMP-activated protein kinase (AMPK) pathway, HPA-s were obtained and divided in...

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Autores principales: Su, MiaoShang, He, Yifan, Xue, Sichen, Yu, Jueke, Ren, Xikai, Huang, Nan, Abdullahi, Rukkaiya, Xu, Manhuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8220371/
https://www.ncbi.nlm.nih.gov/pubmed/33876818
http://dx.doi.org/10.1042/BSR20203639
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author Su, MiaoShang
He, Yifan
Xue, Sichen
Yu, Jueke
Ren, Xikai
Huang, Nan
Abdullahi, Rukkaiya
Xu, Manhuan
author_facet Su, MiaoShang
He, Yifan
Xue, Sichen
Yu, Jueke
Ren, Xikai
Huang, Nan
Abdullahi, Rukkaiya
Xu, Manhuan
author_sort Su, MiaoShang
collection PubMed
description To investigate whether butyric acid could alleviate chronic intermittent hypoxia (CIH)-induced lipid formation in human preadipocytes-subcutaneous (HPA-s) through accumulation of human antigen R (HuR) and inactivation of AMP-activated protein kinase (AMPK) pathway, HPA-s were obtained and divided into three groups: Control group: cells were cultured under normal conditions; CIH group: cells were cultured in a three-gas incubator (10% O(2)); Butyric acid group: 10 mmol/l butyric acid added into cell culture medium. HuR-siRNA was futher transfected into CIH group for verification the function of HuR. Oil Red O was implemented for observation of lipid droplets within cells. Cell Counting Kit-8 (CCK8) assay was used for detecting cell viability. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-nick end labeling (TUNEL) assay as well as flow cytometry analysis was employed for determining cell apoptosis. Western blotting was used for measurement of protein expression levels. RT-qPCR analysis was used for detecting mRNA expression. CIH treatment increased adipocytes proliferation, while butyric acid inhibited cell proliferation and promoted cell apoptosis. The treatment of butyric acid in CIH group down-regulated expression of inflammatory factors and increased cell apoptotic rate. Butyric acid treatment increased HuR expression in both cytoplasm and nucleus and decreased the level of p-AMPK and p-ACC, while transfection of AMPK activator or HuR-siRNA would down-regulate HuR expression. Moreover, butyric acid alleviated CIH-induced cell proliferation, lipid formation and inflammatory status and promoted cell apoptosis through regulating related genes including p21, PPARγ, C/EBPa, IL-1β, IL-6, TLR4, caspase-8 and caspase-3. In conclusion, butyric acid could alleviate CIH-induced inflammation, cell proliferation and lipid formation through accumulation of HuR and inactivation of AMPK pathway.
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spelling pubmed-82203712021-07-07 Butyric acid alleviated chronic intermittent hypoxia-induced lipid formation and inflammation through up-regulating HuR expression and inactivating AMPK pathways Su, MiaoShang He, Yifan Xue, Sichen Yu, Jueke Ren, Xikai Huang, Nan Abdullahi, Rukkaiya Xu, Manhuan Biosci Rep Cell Death & Injury To investigate whether butyric acid could alleviate chronic intermittent hypoxia (CIH)-induced lipid formation in human preadipocytes-subcutaneous (HPA-s) through accumulation of human antigen R (HuR) and inactivation of AMP-activated protein kinase (AMPK) pathway, HPA-s were obtained and divided into three groups: Control group: cells were cultured under normal conditions; CIH group: cells were cultured in a three-gas incubator (10% O(2)); Butyric acid group: 10 mmol/l butyric acid added into cell culture medium. HuR-siRNA was futher transfected into CIH group for verification the function of HuR. Oil Red O was implemented for observation of lipid droplets within cells. Cell Counting Kit-8 (CCK8) assay was used for detecting cell viability. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-nick end labeling (TUNEL) assay as well as flow cytometry analysis was employed for determining cell apoptosis. Western blotting was used for measurement of protein expression levels. RT-qPCR analysis was used for detecting mRNA expression. CIH treatment increased adipocytes proliferation, while butyric acid inhibited cell proliferation and promoted cell apoptosis. The treatment of butyric acid in CIH group down-regulated expression of inflammatory factors and increased cell apoptotic rate. Butyric acid treatment increased HuR expression in both cytoplasm and nucleus and decreased the level of p-AMPK and p-ACC, while transfection of AMPK activator or HuR-siRNA would down-regulate HuR expression. Moreover, butyric acid alleviated CIH-induced cell proliferation, lipid formation and inflammatory status and promoted cell apoptosis through regulating related genes including p21, PPARγ, C/EBPa, IL-1β, IL-6, TLR4, caspase-8 and caspase-3. In conclusion, butyric acid could alleviate CIH-induced inflammation, cell proliferation and lipid formation through accumulation of HuR and inactivation of AMPK pathway. Portland Press Ltd. 2021-06-21 /pmc/articles/PMC8220371/ /pubmed/33876818 http://dx.doi.org/10.1042/BSR20203639 Text en © 2021 The Author(s). https://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Cell Death & Injury
Su, MiaoShang
He, Yifan
Xue, Sichen
Yu, Jueke
Ren, Xikai
Huang, Nan
Abdullahi, Rukkaiya
Xu, Manhuan
Butyric acid alleviated chronic intermittent hypoxia-induced lipid formation and inflammation through up-regulating HuR expression and inactivating AMPK pathways
title Butyric acid alleviated chronic intermittent hypoxia-induced lipid formation and inflammation through up-regulating HuR expression and inactivating AMPK pathways
title_full Butyric acid alleviated chronic intermittent hypoxia-induced lipid formation and inflammation through up-regulating HuR expression and inactivating AMPK pathways
title_fullStr Butyric acid alleviated chronic intermittent hypoxia-induced lipid formation and inflammation through up-regulating HuR expression and inactivating AMPK pathways
title_full_unstemmed Butyric acid alleviated chronic intermittent hypoxia-induced lipid formation and inflammation through up-regulating HuR expression and inactivating AMPK pathways
title_short Butyric acid alleviated chronic intermittent hypoxia-induced lipid formation and inflammation through up-regulating HuR expression and inactivating AMPK pathways
title_sort butyric acid alleviated chronic intermittent hypoxia-induced lipid formation and inflammation through up-regulating hur expression and inactivating ampk pathways
topic Cell Death & Injury
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8220371/
https://www.ncbi.nlm.nih.gov/pubmed/33876818
http://dx.doi.org/10.1042/BSR20203639
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