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N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide
Oxidative stress plays an important role in the pathogenesis of liver diseases. N-Acetyl-serotonin (NAS) has been reported to protect against oxidative damage, though the mechanisms by which NAS protects hepatocytes from oxidative stress remain unknown. To determine whether pretreatment with NAS cou...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074966/ https://www.ncbi.nlm.nih.gov/pubmed/25013541 http://dx.doi.org/10.1155/2014/310504 |
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author | Jiang, Jiying Yu, Shuna Jiang, Zhengchen Liang, Cuihong Yu, Wenbo Li, Jin Du, Xiaodong Wang, Hailiang Gao, Xianghong Wang, Xin |
author_facet | Jiang, Jiying Yu, Shuna Jiang, Zhengchen Liang, Cuihong Yu, Wenbo Li, Jin Du, Xiaodong Wang, Hailiang Gao, Xianghong Wang, Xin |
author_sort | Jiang, Jiying |
collection | PubMed |
description | Oxidative stress plays an important role in the pathogenesis of liver diseases. N-Acetyl-serotonin (NAS) has been reported to protect against oxidative damage, though the mechanisms by which NAS protects hepatocytes from oxidative stress remain unknown. To determine whether pretreatment with NAS could reduce hydrogen peroxide- (H(2)O(2)-) induced oxidative stress in HepG2 cells by inhibiting the mitochondrial apoptosis pathway, we investigated the H(2)O(2)-induced oxidative damage to HepG2 cells with or without NAS using MTT, Hoechst 33342, rhodamine 123, Terminal dUTP Nick End Labeling Assay (TUNEL), dihydrodichlorofluorescein (H2DCF), Annexin V and propidium iodide (PI) double staining, immunocytochemistry, and western blot. H(2)O(2) produced dramatic injuries in HepG2 cells, represented by classical morphological changes of apoptosis, increased levels of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS), decreased activity of superoxide dismutase (SOD), and increased activities of caspase-9 and caspase-3, release of cytochrome c (Cyt-C) and apoptosis-inducing factor (AIF) from mitochondria, and loss of membrane potential (ΔΨ(m)). NAS significantly inhibited H(2)O(2)-induced changes, indicating that it protected against H(2)O(2)-induced oxidative damage by reducing MDA levels and increasing SOD activity and that it protected the HepG2 cells from apoptosis through regulating the mitochondrial apoptosis pathway, involving inhibition of mitochondrial hyperpolarization, release of mitochondrial apoptogenic factors, and caspase activity. |
format | Online Article Text |
id | pubmed-4074966 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-40749662014-07-10 N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide Jiang, Jiying Yu, Shuna Jiang, Zhengchen Liang, Cuihong Yu, Wenbo Li, Jin Du, Xiaodong Wang, Hailiang Gao, Xianghong Wang, Xin Oxid Med Cell Longev Research Article Oxidative stress plays an important role in the pathogenesis of liver diseases. N-Acetyl-serotonin (NAS) has been reported to protect against oxidative damage, though the mechanisms by which NAS protects hepatocytes from oxidative stress remain unknown. To determine whether pretreatment with NAS could reduce hydrogen peroxide- (H(2)O(2)-) induced oxidative stress in HepG2 cells by inhibiting the mitochondrial apoptosis pathway, we investigated the H(2)O(2)-induced oxidative damage to HepG2 cells with or without NAS using MTT, Hoechst 33342, rhodamine 123, Terminal dUTP Nick End Labeling Assay (TUNEL), dihydrodichlorofluorescein (H2DCF), Annexin V and propidium iodide (PI) double staining, immunocytochemistry, and western blot. H(2)O(2) produced dramatic injuries in HepG2 cells, represented by classical morphological changes of apoptosis, increased levels of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS), decreased activity of superoxide dismutase (SOD), and increased activities of caspase-9 and caspase-3, release of cytochrome c (Cyt-C) and apoptosis-inducing factor (AIF) from mitochondria, and loss of membrane potential (ΔΨ(m)). NAS significantly inhibited H(2)O(2)-induced changes, indicating that it protected against H(2)O(2)-induced oxidative damage by reducing MDA levels and increasing SOD activity and that it protected the HepG2 cells from apoptosis through regulating the mitochondrial apoptosis pathway, involving inhibition of mitochondrial hyperpolarization, release of mitochondrial apoptogenic factors, and caspase activity. Hindawi Publishing Corporation 2014 2014-06-12 /pmc/articles/PMC4074966/ /pubmed/25013541 http://dx.doi.org/10.1155/2014/310504 Text en Copyright © 2014 Jiying Jiang et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Jiang, Jiying Yu, Shuna Jiang, Zhengchen Liang, Cuihong Yu, Wenbo Li, Jin Du, Xiaodong Wang, Hailiang Gao, Xianghong Wang, Xin N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide |
title | N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide |
title_full | N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide |
title_fullStr | N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide |
title_full_unstemmed | N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide |
title_short | N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide |
title_sort | n-acetyl-serotonin protects hepg2 cells from oxidative stress injury induced by hydrogen peroxide |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074966/ https://www.ncbi.nlm.nih.gov/pubmed/25013541 http://dx.doi.org/10.1155/2014/310504 |
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