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Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway

Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide. Hydrogen sulfide (H(2)S) is involved in a wide range of physiological and pathological processes. Nevertheless, the mechanism of action of H(2)S in NAFLD development has not been fully clarified. Here, the reduced...

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Autores principales: Wu, Dongdong, Zhong, Peiyu, Wang, Yizhen, Zhang, Qianqian, Li, Jianmei, Liu, Zhengguo, Ji, Ailing, Li, Yanzhang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7774297/
https://www.ncbi.nlm.nih.gov/pubmed/33390956
http://dx.doi.org/10.3389/fphar.2020.585860
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author Wu, Dongdong
Zhong, Peiyu
Wang, Yizhen
Zhang, Qianqian
Li, Jianmei
Liu, Zhengguo
Ji, Ailing
Li, Yanzhang
author_facet Wu, Dongdong
Zhong, Peiyu
Wang, Yizhen
Zhang, Qianqian
Li, Jianmei
Liu, Zhengguo
Ji, Ailing
Li, Yanzhang
author_sort Wu, Dongdong
collection PubMed
description Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide. Hydrogen sulfide (H(2)S) is involved in a wide range of physiological and pathological processes. Nevertheless, the mechanism of action of H(2)S in NAFLD development has not been fully clarified. Here, the reduced level of H(2)S was observed in liver cells treated with oleic acid (OA). Administration of H(2)S increased the proliferation of OA-treated cells. The results showed that H(2)S decreased apoptosis and promoted autophagy through reactive oxygen species (ROS)-mediated phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) cascade in OA-treated cells. In addition, administration of H(2)S relieved high-fat diet (HFD)-induced NAFLD via inhibition of apoptosis and promotion of autophagy. These findings suggest that H(2)S could ameliorate HFD-induced NAFLD by regulating apoptosis and autophagy through ROS/PI3K/AKT/mTOR signaling pathway. Novel H(2)S-releasing donors may have therapeutic potential for the treatment of NAFLD.
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spelling pubmed-77742972021-01-01 Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway Wu, Dongdong Zhong, Peiyu Wang, Yizhen Zhang, Qianqian Li, Jianmei Liu, Zhengguo Ji, Ailing Li, Yanzhang Front Pharmacol Pharmacology Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide. Hydrogen sulfide (H(2)S) is involved in a wide range of physiological and pathological processes. Nevertheless, the mechanism of action of H(2)S in NAFLD development has not been fully clarified. Here, the reduced level of H(2)S was observed in liver cells treated with oleic acid (OA). Administration of H(2)S increased the proliferation of OA-treated cells. The results showed that H(2)S decreased apoptosis and promoted autophagy through reactive oxygen species (ROS)-mediated phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) cascade in OA-treated cells. In addition, administration of H(2)S relieved high-fat diet (HFD)-induced NAFLD via inhibition of apoptosis and promotion of autophagy. These findings suggest that H(2)S could ameliorate HFD-induced NAFLD by regulating apoptosis and autophagy through ROS/PI3K/AKT/mTOR signaling pathway. Novel H(2)S-releasing donors may have therapeutic potential for the treatment of NAFLD. Frontiers Media S.A. 2020-11-30 /pmc/articles/PMC7774297/ /pubmed/33390956 http://dx.doi.org/10.3389/fphar.2020.585860 Text en Copyright © 2020 Wu, Zhong, Wang, Zhang, Li, Liu, Ji and Li http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Wu, Dongdong
Zhong, Peiyu
Wang, Yizhen
Zhang, Qianqian
Li, Jianmei
Liu, Zhengguo
Ji, Ailing
Li, Yanzhang
Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway
title Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway
title_full Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway
title_fullStr Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway
title_full_unstemmed Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway
title_short Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway
title_sort hydrogen sulfide attenuates high-fat diet-induced non-alcoholic fatty liver disease by inhibiting apoptosis and promoting autophagy via reactive oxygen species/phosphatidylinositol 3-kinase/akt/mammalian target of rapamycin signaling pathway
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7774297/
https://www.ncbi.nlm.nih.gov/pubmed/33390956
http://dx.doi.org/10.3389/fphar.2020.585860
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