Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study
Imatinib (IM), a milestone drug used in the field of molecular targeted therapy, has been reported to cause serious adverse liver effects, including liver failure and even death. Immune-mediated injury and mitochondrial dysfunction are involved in drug-induced liver injury. However, the mechanism of...
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Veröffentlicht in: | Archives of toxicology 2022-04, Vol.96 (4), p.1075-1087 |
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description | Imatinib (IM), a milestone drug used in the field of molecular targeted therapy, has been reported to cause serious adverse liver effects, including liver failure and even death. Immune-mediated injury and mitochondrial dysfunction are involved in drug-induced liver injury. However, the mechanism of IM-induced hepatotoxicity remains unclear and warrants further study. In our study, Sprague Dawley rats were administered IM by gavage with 50 mg/kg body weight (BW) once daily for 10 days. Drug-induced liver injury accompanied by inflammatory infiltration was observed in rats following IM exposure, and the expression of NOD-like receptor protein 3 (NLRP3) inflammasome-related proteins was significantly increased compared with that of the control. HepG2 cells were exposed to 0–100 μM IM for 24 h. The results showed that IM decreased cell viability in a dose-dependent manner. Moreover, IM induced a state of obvious oxidative stress and activation of nuclear factor kappa B (NF-κB) in cells, which resulted in the activation of NLRP3 inflammasomes, including caspase 1 cleavage and IL-1β release. These results were significantly reduced after the use of the antioxidants N-acetyl-l-cysteine or the NF-κB inhibitor pyrrolidine di-thio-carbamate. Furthermore, NLRP3 knockdown significantly reduced the release of inflammatory cytokines and improved cell viability. In summary, our data demonstrated that oxidative stress and NLRP3 inflammasome activation are involved in the process of IM-induced hepatotoxicity. The results of this study provide a reference for the prevention and treatment of IM-induced hepatotoxicity. |
doi_str_mv | 10.1007/s00204-022-03245-x |
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Immune-mediated injury and mitochondrial dysfunction are involved in drug-induced liver injury. However, the mechanism of IM-induced hepatotoxicity remains unclear and warrants further study. In our study, Sprague Dawley rats were administered IM by gavage with 50 mg/kg body weight (BW) once daily for 10 days. Drug-induced liver injury accompanied by inflammatory infiltration was observed in rats following IM exposure, and the expression of NOD-like receptor protein 3 (NLRP3) inflammasome-related proteins was significantly increased compared with that of the control. HepG2 cells were exposed to 0–100 μM IM for 24 h. The results showed that IM decreased cell viability in a dose-dependent manner. Moreover, IM induced a state of obvious oxidative stress and activation of nuclear factor kappa B (NF-κB) in cells, which resulted in the activation of NLRP3 inflammasomes, including caspase 1 cleavage and IL-1β release. These results were significantly reduced after the use of the antioxidants N-acetyl-l-cysteine or the NF-κB inhibitor pyrrolidine di-thio-carbamate. Furthermore, NLRP3 knockdown significantly reduced the release of inflammatory cytokines and improved cell viability. In summary, our data demonstrated that oxidative stress and NLRP3 inflammasome activation are involved in the process of IM-induced hepatotoxicity. The results of this study provide a reference for the prevention and treatment of IM-induced hepatotoxicity.</description><identifier>ISSN: 0340-5761</identifier><identifier>EISSN: 1432-0738</identifier><identifier>DOI: 10.1007/s00204-022-03245-x</identifier><identifier>PMID: 35190838</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Antioxidants ; Biomedical and Life Sciences ; Biomedicine ; Body weight ; Caspase-1 ; Cell viability ; Chemical and Drug Induced Liver Injury - etiology ; Cytokines ; Environmental Health ; Hepatotoxicity ; IL-1β ; Imatinib ; Imatinib Mesylate - pharmacology ; In vivo methods and tests ; Inflammasomes ; Inflammation ; Injuries ; Liver ; Liver diseases ; Mitochondria ; N-Acetyl-L-cysteine ; NF-kappa B - metabolism ; NF-κB protein ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLR Proteins - metabolism ; Occupational Medicine/Industrial Medicine ; Organ Toxicity and Mechanisms ; Oxidative Stress ; Pharmacology/Toxicology ; Proteins ; Pyrrolidine ; Rats ; Rats, Sprague-Dawley</subject><ispartof>Archives of toxicology, 2022-04, Vol.96 (4), p.1075-1087</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-57dc64c265e27c97fa2109e753504509af821e7e056fa9360e8cd403cc9640b73</citedby><cites>FETCH-LOGICAL-c375t-57dc64c265e27c97fa2109e753504509af821e7e056fa9360e8cd403cc9640b73</cites><orcidid>0000-0001-8340-6003</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00204-022-03245-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00204-022-03245-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35190838$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Feng-Ru</creatorcontrib><creatorcontrib>Fang, Wen-Tong</creatorcontrib><creatorcontrib>Cheng, Zi-Ping</creatorcontrib><creatorcontrib>Shen, Ye</creatorcontrib><creatorcontrib>Wang, Dun-Jian</creatorcontrib><creatorcontrib>Wang, Yong-Qing</creatorcontrib><creatorcontrib>Sun, Lu-Ning</creatorcontrib><title>Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study</title><title>Archives of toxicology</title><addtitle>Arch Toxicol</addtitle><addtitle>Arch Toxicol</addtitle><description>Imatinib (IM), a milestone drug used in the field of molecular targeted therapy, has been reported to cause serious adverse liver effects, including liver failure and even death. Immune-mediated injury and mitochondrial dysfunction are involved in drug-induced liver injury. However, the mechanism of IM-induced hepatotoxicity remains unclear and warrants further study. In our study, Sprague Dawley rats were administered IM by gavage with 50 mg/kg body weight (BW) once daily for 10 days. Drug-induced liver injury accompanied by inflammatory infiltration was observed in rats following IM exposure, and the expression of NOD-like receptor protein 3 (NLRP3) inflammasome-related proteins was significantly increased compared with that of the control. HepG2 cells were exposed to 0–100 μM IM for 24 h. The results showed that IM decreased cell viability in a dose-dependent manner. Moreover, IM induced a state of obvious oxidative stress and activation of nuclear factor kappa B (NF-κB) in cells, which resulted in the activation of NLRP3 inflammasomes, including caspase 1 cleavage and IL-1β release. These results were significantly reduced after the use of the antioxidants N-acetyl-l-cysteine or the NF-κB inhibitor pyrrolidine di-thio-carbamate. Furthermore, NLRP3 knockdown significantly reduced the release of inflammatory cytokines and improved cell viability. In summary, our data demonstrated that oxidative stress and NLRP3 inflammasome activation are involved in the process of IM-induced hepatotoxicity. The results of this study provide a reference for the prevention and treatment of IM-induced hepatotoxicity.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Body weight</subject><subject>Caspase-1</subject><subject>Cell viability</subject><subject>Chemical and Drug Induced Liver Injury - etiology</subject><subject>Cytokines</subject><subject>Environmental Health</subject><subject>Hepatotoxicity</subject><subject>IL-1β</subject><subject>Imatinib</subject><subject>Imatinib Mesylate - pharmacology</subject><subject>In vivo methods and tests</subject><subject>Inflammasomes</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Mitochondria</subject><subject>N-Acetyl-L-cysteine</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLR Proteins - metabolism</subject><subject>Occupational Medicine/Industrial Medicine</subject><subject>Organ Toxicity and Mechanisms</subject><subject>Oxidative Stress</subject><subject>Pharmacology/Toxicology</subject><subject>Proteins</subject><subject>Pyrrolidine</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>0340-5761</issn><issn>1432-0738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kUtvEzEUha0K1IbSP9AFssSGzbTXbw87VPGoFBWEYG05Hg-4yoyDPRMl_57bpAWJBSv7Hn_n-EqHkEsGVwzAXFcADrIBzhsQXKpmd0IWTAocjbDPyAKEhEYZzc7Ii1rvARi3rTglZ0KxFqywC7K7HfyUxrRq0tjNIXb0Z9z4KU95l0Ka9nSbPMV7h9Q20jqVWCv1Y0d9QAXVPNLc07vl1y-CprFf-2HwNQ_xLVIoYMBU8sFxGLYZQ-Zu_5I87_26xovH85x8__D-282nZvn54-3Nu2UThFETbt8FLQPXKnITWtN7zqCNRgkFUkHre8tZNBGU7n0rNEQbOgkihFZLWBlxTt4cczcl_5pjndyQaojrtR9jnqvjWjCrpQSN6Ot_0Ps8lxG3e6CsVdIAQ4ofqVByrSX2blPS4MveMXAPvbhjLw57cYde3A5Nrx6j59UQuz-WpyIQEEeg4tP4I5a_f_8n9jfFgZjh</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Huang, Feng-Ru</creator><creator>Fang, Wen-Tong</creator><creator>Cheng, Zi-Ping</creator><creator>Shen, Ye</creator><creator>Wang, Dun-Jian</creator><creator>Wang, Yong-Qing</creator><creator>Sun, Lu-Ning</creator><general>Springer Berlin Heidelberg</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>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T2</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8340-6003</orcidid></search><sort><creationdate>20220401</creationdate><title>Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study</title><author>Huang, Feng-Ru ; Fang, Wen-Tong ; Cheng, Zi-Ping ; Shen, Ye ; Wang, Dun-Jian ; Wang, Yong-Qing ; Sun, Lu-Ning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-57dc64c265e27c97fa2109e753504509af821e7e056fa9360e8cd403cc9640b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Body weight</topic><topic>Caspase-1</topic><topic>Cell viability</topic><topic>Chemical and Drug Induced Liver Injury - etiology</topic><topic>Cytokines</topic><topic>Environmental Health</topic><topic>Hepatotoxicity</topic><topic>IL-1β</topic><topic>Imatinib</topic><topic>Imatinib Mesylate - pharmacology</topic><topic>In vivo methods and tests</topic><topic>Inflammasomes</topic><topic>Inflammation</topic><topic>Injuries</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>Mitochondria</topic><topic>N-Acetyl-L-cysteine</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLR Proteins - metabolism</topic><topic>Occupational Medicine/Industrial Medicine</topic><topic>Organ Toxicity and Mechanisms</topic><topic>Oxidative Stress</topic><topic>Pharmacology/Toxicology</topic><topic>Proteins</topic><topic>Pyrrolidine</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Feng-Ru</creatorcontrib><creatorcontrib>Fang, Wen-Tong</creatorcontrib><creatorcontrib>Cheng, Zi-Ping</creatorcontrib><creatorcontrib>Shen, Ye</creatorcontrib><creatorcontrib>Wang, Dun-Jian</creatorcontrib><creatorcontrib>Wang, Yong-Qing</creatorcontrib><creatorcontrib>Sun, Lu-Ning</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Feng-Ru</au><au>Fang, Wen-Tong</au><au>Cheng, Zi-Ping</au><au>Shen, Ye</au><au>Wang, Dun-Jian</au><au>Wang, Yong-Qing</au><au>Sun, Lu-Ning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study</atitle><jtitle>Archives of toxicology</jtitle><stitle>Arch Toxicol</stitle><addtitle>Arch Toxicol</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>96</volume><issue>4</issue><spage>1075</spage><epage>1087</epage><pages>1075-1087</pages><issn>0340-5761</issn><eissn>1432-0738</eissn><abstract>Imatinib (IM), a milestone drug used in the field of molecular targeted therapy, has been reported to cause serious adverse liver effects, including liver failure and even death. Immune-mediated injury and mitochondrial dysfunction are involved in drug-induced liver injury. However, the mechanism of IM-induced hepatotoxicity remains unclear and warrants further study. In our study, Sprague Dawley rats were administered IM by gavage with 50 mg/kg body weight (BW) once daily for 10 days. Drug-induced liver injury accompanied by inflammatory infiltration was observed in rats following IM exposure, and the expression of NOD-like receptor protein 3 (NLRP3) inflammasome-related proteins was significantly increased compared with that of the control. HepG2 cells were exposed to 0–100 μM IM for 24 h. The results showed that IM decreased cell viability in a dose-dependent manner. Moreover, IM induced a state of obvious oxidative stress and activation of nuclear factor kappa B (NF-κB) in cells, which resulted in the activation of NLRP3 inflammasomes, including caspase 1 cleavage and IL-1β release. These results were significantly reduced after the use of the antioxidants N-acetyl-l-cysteine or the NF-κB inhibitor pyrrolidine di-thio-carbamate. Furthermore, NLRP3 knockdown significantly reduced the release of inflammatory cytokines and improved cell viability. In summary, our data demonstrated that oxidative stress and NLRP3 inflammasome activation are involved in the process of IM-induced hepatotoxicity. The results of this study provide a reference for the prevention and treatment of IM-induced hepatotoxicity.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>35190838</pmid><doi>10.1007/s00204-022-03245-x</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-8340-6003</orcidid></addata></record> |
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subjects | Animals Antioxidants Biomedical and Life Sciences Biomedicine Body weight Caspase-1 Cell viability Chemical and Drug Induced Liver Injury - etiology Cytokines Environmental Health Hepatotoxicity IL-1β Imatinib Imatinib Mesylate - pharmacology In vivo methods and tests Inflammasomes Inflammation Injuries Liver Liver diseases Mitochondria N-Acetyl-L-cysteine NF-kappa B - metabolism NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLR Proteins - metabolism Occupational Medicine/Industrial Medicine Organ Toxicity and Mechanisms Oxidative Stress Pharmacology/Toxicology Proteins Pyrrolidine Rats Rats, Sprague-Dawley |
title | Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study |
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