Efect of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells
Non-alcoholic fatty liver disease is a prevalent liver condition that can progress to fibrosis and cirrhosis. It also poses a risk for hepatocellular carcinoma, underscoring the importance of identifying effective treatments. N-acetylcysteine, an inhibitor of glutathione depletion, shows promise in...
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| Veröffentlicht in: | Journal of molecular histology 2025-02, Vol.56 (1), p.27 |
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| creator | Gholamrezapour, Mohammadreza Taghizadeh Ghavamabadi, Raziyeh Taghavi, Mohammad Mohsen Dehghani Soltani, Samereh Shabanizadeh, Ahmad Vazirinejad, Reza Taghipour, Zahra |
| description | Non-alcoholic fatty liver disease is a prevalent liver condition that can progress to fibrosis and cirrhosis. It also poses a risk for hepatocellular carcinoma, underscoring the importance of identifying effective treatments. N-acetylcysteine, an inhibitor of glutathione depletion, shows promise in modulating intracellular glutathione biosynthesis and combating oxidative stress, making it a potentially beneficial therapy for liver fibrosis in non-alcoholic fatty liver disease. This study assesses the impact of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells was evaluated. HepG2 cells were cultured in DMEM and seeded onto six-well plates at a density of 5 × 10
5
cells. Following a 24-h incubation period, the cells were exposed to a medium inducing fat accumulation. Subsequently, the cells were treated with varying concentrations of N-acetylcysteine for 48 h. Some plates were utilized for Real-Time-PCR tests, while others underwent Oil Red staining. The findings indicated a significant increase in the expression of fatty acid β-oxidation genes in the group treated with 10mM N-acetylcysteine (p |
| doi_str_mv | 10.1007/s10735-024-10313-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_3140930431</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3140763594</sourcerecordid><originalsourceid>FETCH-LOGICAL-p213t-65faabb3eb50c2812356647abde9c4a64cdee1f7c73ab0e9aa1f1cda7d261be23</originalsourceid><addsrcrecordid>eNpdkUtLw0AUhQdRbK3-ARcy4MbN6Lwy0yyl1FYoCqLrYTK5sSlpEjMTS_69aeMDXJ0L9-NwOAehS0ZvGaX6zjOqRUQol4RRwQThR2jMIqUJF1N9_HvreITOvN9QyqdKxqdoJGIlKNN0jF7mGbiAqww_EesgdIXrfIC8BFyVeAn1gmMHReHxbp27Nd5BAzgv09ZB2muocGZD6HCRf0IzkOfoJLOFh4tvnaC3h_nrbElWz4vH2f2K1JyJQFSUWZskApKIOj5lXERKSW2TFGInrZIuBWCZdlrYhEJsLcuYS61OuWIJcDFBN4Nv3VQfLfhgtrnfJ7AlVK03gkkaCyr7Zibo-h-6qdqm7NMdKK1EFMueuvqm2mQLqambfGubzvy01QNiAHz_Kt-h-bNh1Ow3McMmpt_EHDYxXHwBE-N76w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3140763594</pqid></control><display><type>article</type><title>Efect of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Gholamrezapour, Mohammadreza ; Taghizadeh Ghavamabadi, Raziyeh ; Taghavi, Mohammad Mohsen ; Dehghani Soltani, Samereh ; Shabanizadeh, Ahmad ; Vazirinejad, Reza ; Taghipour, Zahra</creator><creatorcontrib>Gholamrezapour, Mohammadreza ; Taghizadeh Ghavamabadi, Raziyeh ; Taghavi, Mohammad Mohsen ; Dehghani Soltani, Samereh ; Shabanizadeh, Ahmad ; Vazirinejad, Reza ; Taghipour, Zahra</creatorcontrib><description>Non-alcoholic fatty liver disease is a prevalent liver condition that can progress to fibrosis and cirrhosis. It also poses a risk for hepatocellular carcinoma, underscoring the importance of identifying effective treatments. N-acetylcysteine, an inhibitor of glutathione depletion, shows promise in modulating intracellular glutathione biosynthesis and combating oxidative stress, making it a potentially beneficial therapy for liver fibrosis in non-alcoholic fatty liver disease. This study assesses the impact of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells was evaluated. HepG2 cells were cultured in DMEM and seeded onto six-well plates at a density of 5 × 10
5
cells. Following a 24-h incubation period, the cells were exposed to a medium inducing fat accumulation. Subsequently, the cells were treated with varying concentrations of N-acetylcysteine for 48 h. Some plates were utilized for Real-Time-PCR tests, while others underwent Oil Red staining. The findings indicated a significant increase in the expression of fatty acid β-oxidation genes in the group treated with 10mM N-acetylcysteine (p < 0.05), along with reduced expression of lipogenesis-related genes (p < 0.05) in N-acetylcysteine-treated groups. Analysis of apoptotic gene expression revealed decreased
BAX
expression but increased
BCL2
expression in the N-acetylcysteine-treated groups. Oil Red staining demonstrated a dose-dependent reduction in lipid droplets compared to the control group. This study's results suggest that N-acetylcysteine has the potential to decrease lipid droplets and modulate lipid metabolism effectively.
Graphical abstract</description><identifier>ISSN: 1567-2379</identifier><identifier>ISSN: 1567-2387</identifier><identifier>EISSN: 1567-2387</identifier><identifier>DOI: 10.1007/s10735-024-10313-2</identifier><identifier>PMID: 39630170</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Acetylcysteine ; Acetylcysteine - pharmacology ; Apoptosis ; Apoptosis - drug effects ; BAX protein ; Bcl-2 protein ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cirrhosis ; Developmental Biology ; Fatty liver ; Fatty Liver - metabolism ; Fatty Liver - pathology ; Fibrosis ; Gene expression ; Gene Expression Regulation - drug effects ; Glutathione ; Glutathione - metabolism ; Hep G2 Cells ; Hepatocellular carcinoma ; Hepatocytes ; Humans ; Life Sciences ; Lipid metabolism ; Lipid Metabolism - drug effects ; Lipids ; Lipogenesis ; Lipogenesis - drug effects ; Liver diseases ; Non-alcoholic Fatty Liver Disease - drug therapy ; Non-alcoholic Fatty Liver Disease - metabolism ; Non-alcoholic Fatty Liver Disease - pathology ; Original Paper ; Oxidative stress ; Oxidative Stress - drug effects</subject><ispartof>Journal of molecular histology, 2025-02, Vol.56 (1), p.27</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2024 Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer Nature B.V.</rights><rights>Copyright Springer Nature B.V. Feb 2025</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10735-024-10313-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10735-024-10313-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39630170$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gholamrezapour, Mohammadreza</creatorcontrib><creatorcontrib>Taghizadeh Ghavamabadi, Raziyeh</creatorcontrib><creatorcontrib>Taghavi, Mohammad Mohsen</creatorcontrib><creatorcontrib>Dehghani Soltani, Samereh</creatorcontrib><creatorcontrib>Shabanizadeh, Ahmad</creatorcontrib><creatorcontrib>Vazirinejad, Reza</creatorcontrib><creatorcontrib>Taghipour, Zahra</creatorcontrib><title>Efect of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells</title><title>Journal of molecular histology</title><addtitle>J Mol Histol</addtitle><addtitle>J Mol Histol</addtitle><description>Non-alcoholic fatty liver disease is a prevalent liver condition that can progress to fibrosis and cirrhosis. It also poses a risk for hepatocellular carcinoma, underscoring the importance of identifying effective treatments. N-acetylcysteine, an inhibitor of glutathione depletion, shows promise in modulating intracellular glutathione biosynthesis and combating oxidative stress, making it a potentially beneficial therapy for liver fibrosis in non-alcoholic fatty liver disease. This study assesses the impact of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells was evaluated. HepG2 cells were cultured in DMEM and seeded onto six-well plates at a density of 5 × 10
5
cells. Following a 24-h incubation period, the cells were exposed to a medium inducing fat accumulation. Subsequently, the cells were treated with varying concentrations of N-acetylcysteine for 48 h. Some plates were utilized for Real-Time-PCR tests, while others underwent Oil Red staining. The findings indicated a significant increase in the expression of fatty acid β-oxidation genes in the group treated with 10mM N-acetylcysteine (p < 0.05), along with reduced expression of lipogenesis-related genes (p < 0.05) in N-acetylcysteine-treated groups. Analysis of apoptotic gene expression revealed decreased
BAX
expression but increased
BCL2
expression in the N-acetylcysteine-treated groups. Oil Red staining demonstrated a dose-dependent reduction in lipid droplets compared to the control group. This study's results suggest that N-acetylcysteine has the potential to decrease lipid droplets and modulate lipid metabolism effectively.
Graphical abstract</description><subject>Acetylcysteine</subject><subject>Acetylcysteine - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cirrhosis</subject><subject>Developmental Biology</subject><subject>Fatty liver</subject><subject>Fatty Liver - metabolism</subject><subject>Fatty Liver - pathology</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glutathione</subject><subject>Glutathione - metabolism</subject><subject>Hep G2 Cells</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatocytes</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Lipid metabolism</subject><subject>Lipid Metabolism - drug effects</subject><subject>Lipids</subject><subject>Lipogenesis</subject><subject>Lipogenesis - drug effects</subject><subject>Liver diseases</subject><subject>Non-alcoholic Fatty Liver Disease - drug therapy</subject><subject>Non-alcoholic Fatty Liver Disease - metabolism</subject><subject>Non-alcoholic Fatty Liver Disease - pathology</subject><subject>Original Paper</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><issn>1567-2379</issn><issn>1567-2387</issn><issn>1567-2387</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUtLw0AUhQdRbK3-ARcy4MbN6Lwy0yyl1FYoCqLrYTK5sSlpEjMTS_69aeMDXJ0L9-NwOAehS0ZvGaX6zjOqRUQol4RRwQThR2jMIqUJF1N9_HvreITOvN9QyqdKxqdoJGIlKNN0jF7mGbiAqww_EesgdIXrfIC8BFyVeAn1gmMHReHxbp27Nd5BAzgv09ZB2muocGZD6HCRf0IzkOfoJLOFh4tvnaC3h_nrbElWz4vH2f2K1JyJQFSUWZskApKIOj5lXERKSW2TFGInrZIuBWCZdlrYhEJsLcuYS61OuWIJcDFBN4Nv3VQfLfhgtrnfJ7AlVK03gkkaCyr7Zibo-h-6qdqm7NMdKK1EFMueuvqm2mQLqambfGubzvy01QNiAHz_Kt-h-bNh1Ow3McMmpt_EHDYxXHwBE-N76w</recordid><startdate>20250201</startdate><enddate>20250201</enddate><creator>Gholamrezapour, Mohammadreza</creator><creator>Taghizadeh Ghavamabadi, Raziyeh</creator><creator>Taghavi, Mohammad Mohsen</creator><creator>Dehghani Soltani, Samereh</creator><creator>Shabanizadeh, Ahmad</creator><creator>Vazirinejad, Reza</creator><creator>Taghipour, Zahra</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20250201</creationdate><title>Efect of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells</title><author>Gholamrezapour, Mohammadreza ; Taghizadeh Ghavamabadi, Raziyeh ; Taghavi, Mohammad Mohsen ; Dehghani Soltani, Samereh ; Shabanizadeh, Ahmad ; Vazirinejad, Reza ; Taghipour, Zahra</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p213t-65faabb3eb50c2812356647abde9c4a64cdee1f7c73ab0e9aa1f1cda7d261be23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2025</creationdate><topic>Acetylcysteine</topic><topic>Acetylcysteine - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cirrhosis</topic><topic>Developmental Biology</topic><topic>Fatty liver</topic><topic>Fatty Liver - metabolism</topic><topic>Fatty Liver - pathology</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glutathione</topic><topic>Glutathione - metabolism</topic><topic>Hep G2 Cells</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatocytes</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Lipid metabolism</topic><topic>Lipid Metabolism - drug effects</topic><topic>Lipids</topic><topic>Lipogenesis</topic><topic>Lipogenesis - drug effects</topic><topic>Liver diseases</topic><topic>Non-alcoholic Fatty Liver Disease - drug therapy</topic><topic>Non-alcoholic Fatty Liver Disease - metabolism</topic><topic>Non-alcoholic Fatty Liver Disease - pathology</topic><topic>Original Paper</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gholamrezapour, Mohammadreza</creatorcontrib><creatorcontrib>Taghizadeh Ghavamabadi, Raziyeh</creatorcontrib><creatorcontrib>Taghavi, Mohammad Mohsen</creatorcontrib><creatorcontrib>Dehghani Soltani, Samereh</creatorcontrib><creatorcontrib>Shabanizadeh, Ahmad</creatorcontrib><creatorcontrib>Vazirinejad, Reza</creatorcontrib><creatorcontrib>Taghipour, Zahra</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular histology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gholamrezapour, Mohammadreza</au><au>Taghizadeh Ghavamabadi, Raziyeh</au><au>Taghavi, Mohammad Mohsen</au><au>Dehghani Soltani, Samereh</au><au>Shabanizadeh, Ahmad</au><au>Vazirinejad, Reza</au><au>Taghipour, Zahra</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Efect of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells</atitle><jtitle>Journal of molecular histology</jtitle><stitle>J Mol Histol</stitle><addtitle>J Mol Histol</addtitle><date>2025-02-01</date><risdate>2025</risdate><volume>56</volume><issue>1</issue><spage>27</spage><pages>27-</pages><issn>1567-2379</issn><issn>1567-2387</issn><eissn>1567-2387</eissn><abstract>Non-alcoholic fatty liver disease is a prevalent liver condition that can progress to fibrosis and cirrhosis. It also poses a risk for hepatocellular carcinoma, underscoring the importance of identifying effective treatments. N-acetylcysteine, an inhibitor of glutathione depletion, shows promise in modulating intracellular glutathione biosynthesis and combating oxidative stress, making it a potentially beneficial therapy for liver fibrosis in non-alcoholic fatty liver disease. This study assesses the impact of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells was evaluated. HepG2 cells were cultured in DMEM and seeded onto six-well plates at a density of 5 × 10
5
cells. Following a 24-h incubation period, the cells were exposed to a medium inducing fat accumulation. Subsequently, the cells were treated with varying concentrations of N-acetylcysteine for 48 h. Some plates were utilized for Real-Time-PCR tests, while others underwent Oil Red staining. The findings indicated a significant increase in the expression of fatty acid β-oxidation genes in the group treated with 10mM N-acetylcysteine (p < 0.05), along with reduced expression of lipogenesis-related genes (p < 0.05) in N-acetylcysteine-treated groups. Analysis of apoptotic gene expression revealed decreased
BAX
expression but increased
BCL2
expression in the N-acetylcysteine-treated groups. Oil Red staining demonstrated a dose-dependent reduction in lipid droplets compared to the control group. This study's results suggest that N-acetylcysteine has the potential to decrease lipid droplets and modulate lipid metabolism effectively.
Graphical abstract</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>39630170</pmid><doi>10.1007/s10735-024-10313-2</doi></addata></record> |
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| subjects | Acetylcysteine Acetylcysteine - pharmacology Apoptosis Apoptosis - drug effects BAX protein Bcl-2 protein Biomedical and Life Sciences Biomedicine Cell Biology Cirrhosis Developmental Biology Fatty liver Fatty Liver - metabolism Fatty Liver - pathology Fibrosis Gene expression Gene Expression Regulation - drug effects Glutathione Glutathione - metabolism Hep G2 Cells Hepatocellular carcinoma Hepatocytes Humans Life Sciences Lipid metabolism Lipid Metabolism - drug effects Lipids Lipogenesis Lipogenesis - drug effects Liver diseases Non-alcoholic Fatty Liver Disease - drug therapy Non-alcoholic Fatty Liver Disease - metabolism Non-alcoholic Fatty Liver Disease - pathology Original Paper Oxidative stress Oxidative Stress - drug effects |
| title | Efect of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells |
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