5-AIQ inhibits H2O2-induced apoptosis through reactive oxygen species scavenging and Akt/GSK-3β signaling pathway in H9c2 cardiomyocytes
Poly(adenosine 5′-diphosphate ribose) polymerase (PARP) is a nuclear enzyme activated by DNA strand breaks and plays an important role in the tissue injury associated with ischemia and reperfusion. The aim of the present study was to investigate the protective effect of 5-aminoisoquinolinone (5-AIQ)...
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| Veröffentlicht in: | Toxicology and applied pharmacology 2013-04, Vol.268 (1), p.90-98 |
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| creator | Park, Eun-Seok Kang, Jun Chul Kang, Do-Hyun Jang, Yong Chang Yi, Kyu Yang Chung, Hun-Jong Park, Jong Seok Kim, Bokyung Feng, Zhong-Ping Shin, Hwa-Sup |
| description | Poly(adenosine 5′-diphosphate ribose) polymerase (PARP) is a nuclear enzyme activated by DNA strand breaks and plays an important role in the tissue injury associated with ischemia and reperfusion. The aim of the present study was to investigate the protective effect of 5-aminoisoquinolinone (5-AIQ), a PARP inhibitor, against oxidative stress-induced apoptosis in H9c2 cardiomyocytes. 5-AIQ pretreatment significantly protected against H2O2-induced cell death, as determined by the XTT assay, cell counting, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and Western blot analysis of apoptosis-related proteins such as caspase-3, Bax, and Bcl-2. Upregulation of antioxidant enzymes such as manganese superoxide dismutase and catalase accompanied the protective effect of 5-AIQ on H2O2-induced cell death. Our data also showed that 5-AIQ pretreatment protected H9c2 cells from H2O2-induced apoptosis by triggering activation of Akt and glycogen synthase kinase-3β (GSK-3β), and that the protective effect of 5-AIQ was diminished by the PI3K inhibitor LY294002 at a concentration that effectively abolished 5-AIQ-induced Akt and GSK-3β activation. In addition, inhibiting the Akt/GSK-3β pathway by LY294002 significantly attenuated the 5-AIQ-mediated decrease in cleaved caspase-3 and Bax activation and H9c2 cell apoptosis induction. Taken together, these results demonstrate that 5-AIQ prevents H2O2-induced apoptosis in H9c2 cells by reducing intracellular reactive oxygen species production, regulating apoptosis-related proteins, and activating the Akt/GSK-3β pathway.
► 5-AIQ, a PARP inhibitor, decreased H2O2-induced H9c2 cell death and apoptosis. ► 5-AIQ upregulated antioxidant Mn-SOD and catalase, while decreasing ROS production. ► 5-AIQ decreased H2O2-induced increase in cleaved caspase-3 and Bax and decrease in Bcl2. ► 5-AIQ activated Akt and GSK-3β, the effect being abolished by PI3K inhibitor LY294002. ► LY294002 attenuated 5-AIQ-mediated effects on H9c2 apoptosis and related proteins. |
| doi_str_mv | 10.1016/j.taap.2013.01.004 |
| format | Article |
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► 5-AIQ, a PARP inhibitor, decreased H2O2-induced H9c2 cell death and apoptosis. ► 5-AIQ upregulated antioxidant Mn-SOD and catalase, while decreasing ROS production. ► 5-AIQ decreased H2O2-induced increase in cleaved caspase-3 and Bax and decrease in Bcl2. ► 5-AIQ activated Akt and GSK-3β, the effect being abolished by PI3K inhibitor LY294002. ► LY294002 attenuated 5-AIQ-mediated effects on H9c2 apoptosis and related proteins.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2013.01.004</identifier><identifier>PMID: 23352507</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>5-AIQ ; Akt/glycogen synthase kinase-3β ; Animals ; Apoptosis - drug effects ; Biological and medical sciences ; Blotting, Western ; Cell Line ; Cell Survival - drug effects ; Cell Survival - physiology ; Glycogen Synthase Kinase 3 - metabolism ; Glycogen Synthase Kinase 3 beta ; Hydrogen Peroxide - antagonists & inhibitors ; Hydrogen Peroxide - pharmacology ; In Situ Nick-End Labeling ; Isoquinolines - pharmacology ; Medical sciences ; Myocardial apoptosis ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Oxidative Stress - drug effects ; PARP inhibitor ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Signal Transduction - drug effects ; Toxicology</subject><ispartof>Toxicology and applied pharmacology, 2013-04, Vol.268 (1), p.90-98</ispartof><rights>2013 Elsevier Inc.</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-80afdfbb69548d3e776413f939f94bed778113303c8562df23e7be9f204f16c43</citedby><cites>FETCH-LOGICAL-c419t-80afdfbb69548d3e776413f939f94bed778113303c8562df23e7be9f204f16c43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.taap.2013.01.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27194194$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23352507$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Park, Eun-Seok</creatorcontrib><creatorcontrib>Kang, Jun Chul</creatorcontrib><creatorcontrib>Kang, Do-Hyun</creatorcontrib><creatorcontrib>Jang, Yong Chang</creatorcontrib><creatorcontrib>Yi, Kyu Yang</creatorcontrib><creatorcontrib>Chung, Hun-Jong</creatorcontrib><creatorcontrib>Park, Jong Seok</creatorcontrib><creatorcontrib>Kim, Bokyung</creatorcontrib><creatorcontrib>Feng, Zhong-Ping</creatorcontrib><creatorcontrib>Shin, Hwa-Sup</creatorcontrib><title>5-AIQ inhibits H2O2-induced apoptosis through reactive oxygen species scavenging and Akt/GSK-3β signaling pathway in H9c2 cardiomyocytes</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>Poly(adenosine 5′-diphosphate ribose) polymerase (PARP) is a nuclear enzyme activated by DNA strand breaks and plays an important role in the tissue injury associated with ischemia and reperfusion. The aim of the present study was to investigate the protective effect of 5-aminoisoquinolinone (5-AIQ), a PARP inhibitor, against oxidative stress-induced apoptosis in H9c2 cardiomyocytes. 5-AIQ pretreatment significantly protected against H2O2-induced cell death, as determined by the XTT assay, cell counting, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and Western blot analysis of apoptosis-related proteins such as caspase-3, Bax, and Bcl-2. Upregulation of antioxidant enzymes such as manganese superoxide dismutase and catalase accompanied the protective effect of 5-AIQ on H2O2-induced cell death. Our data also showed that 5-AIQ pretreatment protected H9c2 cells from H2O2-induced apoptosis by triggering activation of Akt and glycogen synthase kinase-3β (GSK-3β), and that the protective effect of 5-AIQ was diminished by the PI3K inhibitor LY294002 at a concentration that effectively abolished 5-AIQ-induced Akt and GSK-3β activation. In addition, inhibiting the Akt/GSK-3β pathway by LY294002 significantly attenuated the 5-AIQ-mediated decrease in cleaved caspase-3 and Bax activation and H9c2 cell apoptosis induction. Taken together, these results demonstrate that 5-AIQ prevents H2O2-induced apoptosis in H9c2 cells by reducing intracellular reactive oxygen species production, regulating apoptosis-related proteins, and activating the Akt/GSK-3β pathway.
► 5-AIQ, a PARP inhibitor, decreased H2O2-induced H9c2 cell death and apoptosis. ► 5-AIQ upregulated antioxidant Mn-SOD and catalase, while decreasing ROS production. ► 5-AIQ decreased H2O2-induced increase in cleaved caspase-3 and Bax and decrease in Bcl2. ► 5-AIQ activated Akt and GSK-3β, the effect being abolished by PI3K inhibitor LY294002. ► LY294002 attenuated 5-AIQ-mediated effects on H9c2 apoptosis and related proteins.</description><subject>5-AIQ</subject><subject>Akt/glycogen synthase kinase-3β</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - physiology</subject><subject>Glycogen Synthase Kinase 3 - metabolism</subject><subject>Glycogen Synthase Kinase 3 beta</subject><subject>Hydrogen Peroxide - antagonists & inhibitors</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>In Situ Nick-End Labeling</subject><subject>Isoquinolines - pharmacology</subject><subject>Medical sciences</subject><subject>Myocardial apoptosis</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Oxidative Stress - drug effects</subject><subject>PARP inhibitor</subject><subject>Poly(ADP-ribose) Polymerase Inhibitors</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Toxicology</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcuKFDEYRoMoTjv6Ai4kG8FN1eRSlw64aQadHhwYRAV3IZVLddrqpExSrfUIvo4P4jOZolvduQok5_-SnA-A5xiVGOHmal8mIcaSIExLhEuEqgdghRFrCkQpfQhWeQcXCK0_X4AnMe4RQqyq8GNwQSitSY3aFfhRF5vb99C6ne1sinBL7klhnZqkVlCMfkw-2gjTLvip38GghUz2qKH_PvfawThqaXWEUYqjdr11PRROwc2XdHXz4V1Bf_2E0fZODMvJKNLum5jzZXDLJIFSBGX9YfZyTjo-BY-MGKJ-dl4vwae3bz5eb4u7-5vb681dISvMUrFGwijTdQ2rq7Wium2bClPDKDOs6rRq2zXGlCIq13VDlCEZ6TQzBFUGN7Kil-DVKXcM_uukY-IHG6UeBuG0nyLHTVMRlMNJRskJlcHHGLThY7AHEWaOEV8q4Hu-VMCXCjjCPAvPQy_O-VN30OrvyB_nGXh5BkTWNpggnLTxH9diln-6BL0-cTrbOFodeMyuXS7GBi0TV97-7x2_AbRMpXY</recordid><startdate>20130401</startdate><enddate>20130401</enddate><creator>Park, Eun-Seok</creator><creator>Kang, Jun Chul</creator><creator>Kang, Do-Hyun</creator><creator>Jang, Yong Chang</creator><creator>Yi, Kyu Yang</creator><creator>Chung, Hun-Jong</creator><creator>Park, Jong Seok</creator><creator>Kim, Bokyung</creator><creator>Feng, Zhong-Ping</creator><creator>Shin, Hwa-Sup</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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>7U7</scope><scope>C1K</scope></search><sort><creationdate>20130401</creationdate><title>5-AIQ inhibits H2O2-induced apoptosis through reactive oxygen species scavenging and Akt/GSK-3β signaling pathway in H9c2 cardiomyocytes</title><author>Park, Eun-Seok ; Kang, Jun Chul ; Kang, Do-Hyun ; Jang, Yong Chang ; Yi, Kyu Yang ; Chung, Hun-Jong ; Park, Jong Seok ; Kim, Bokyung ; Feng, Zhong-Ping ; Shin, Hwa-Sup</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-80afdfbb69548d3e776413f939f94bed778113303c8562df23e7be9f204f16c43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>5-AIQ</topic><topic>Akt/glycogen synthase kinase-3β</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - physiology</topic><topic>Glycogen Synthase Kinase 3 - metabolism</topic><topic>Glycogen Synthase Kinase 3 beta</topic><topic>Hydrogen Peroxide - antagonists & inhibitors</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>In Situ Nick-End Labeling</topic><topic>Isoquinolines - pharmacology</topic><topic>Medical sciences</topic><topic>Myocardial apoptosis</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Oxidative Stress - drug effects</topic><topic>PARP inhibitor</topic><topic>Poly(ADP-ribose) Polymerase Inhibitors</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Park, Eun-Seok</creatorcontrib><creatorcontrib>Kang, Jun Chul</creatorcontrib><creatorcontrib>Kang, Do-Hyun</creatorcontrib><creatorcontrib>Jang, Yong Chang</creatorcontrib><creatorcontrib>Yi, Kyu Yang</creatorcontrib><creatorcontrib>Chung, Hun-Jong</creatorcontrib><creatorcontrib>Park, Jong Seok</creatorcontrib><creatorcontrib>Kim, Bokyung</creatorcontrib><creatorcontrib>Feng, Zhong-Ping</creatorcontrib><creatorcontrib>Shin, Hwa-Sup</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Park, Eun-Seok</au><au>Kang, Jun Chul</au><au>Kang, Do-Hyun</au><au>Jang, Yong Chang</au><au>Yi, Kyu Yang</au><au>Chung, Hun-Jong</au><au>Park, Jong Seok</au><au>Kim, Bokyung</au><au>Feng, Zhong-Ping</au><au>Shin, Hwa-Sup</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>5-AIQ inhibits H2O2-induced apoptosis through reactive oxygen species scavenging and Akt/GSK-3β signaling pathway in H9c2 cardiomyocytes</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2013-04-01</date><risdate>2013</risdate><volume>268</volume><issue>1</issue><spage>90</spage><epage>98</epage><pages>90-98</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>Poly(adenosine 5′-diphosphate ribose) polymerase (PARP) is a nuclear enzyme activated by DNA strand breaks and plays an important role in the tissue injury associated with ischemia and reperfusion. The aim of the present study was to investigate the protective effect of 5-aminoisoquinolinone (5-AIQ), a PARP inhibitor, against oxidative stress-induced apoptosis in H9c2 cardiomyocytes. 5-AIQ pretreatment significantly protected against H2O2-induced cell death, as determined by the XTT assay, cell counting, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and Western blot analysis of apoptosis-related proteins such as caspase-3, Bax, and Bcl-2. Upregulation of antioxidant enzymes such as manganese superoxide dismutase and catalase accompanied the protective effect of 5-AIQ on H2O2-induced cell death. Our data also showed that 5-AIQ pretreatment protected H9c2 cells from H2O2-induced apoptosis by triggering activation of Akt and glycogen synthase kinase-3β (GSK-3β), and that the protective effect of 5-AIQ was diminished by the PI3K inhibitor LY294002 at a concentration that effectively abolished 5-AIQ-induced Akt and GSK-3β activation. In addition, inhibiting the Akt/GSK-3β pathway by LY294002 significantly attenuated the 5-AIQ-mediated decrease in cleaved caspase-3 and Bax activation and H9c2 cell apoptosis induction. Taken together, these results demonstrate that 5-AIQ prevents H2O2-induced apoptosis in H9c2 cells by reducing intracellular reactive oxygen species production, regulating apoptosis-related proteins, and activating the Akt/GSK-3β pathway.
► 5-AIQ, a PARP inhibitor, decreased H2O2-induced H9c2 cell death and apoptosis. ► 5-AIQ upregulated antioxidant Mn-SOD and catalase, while decreasing ROS production. ► 5-AIQ decreased H2O2-induced increase in cleaved caspase-3 and Bax and decrease in Bcl2. ► 5-AIQ activated Akt and GSK-3β, the effect being abolished by PI3K inhibitor LY294002. ► LY294002 attenuated 5-AIQ-mediated effects on H9c2 apoptosis and related proteins.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>23352507</pmid><doi>10.1016/j.taap.2013.01.004</doi><tpages>9</tpages></addata></record> |
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| subjects | 5-AIQ Akt/glycogen synthase kinase-3β Animals Apoptosis - drug effects Biological and medical sciences Blotting, Western Cell Line Cell Survival - drug effects Cell Survival - physiology Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta Hydrogen Peroxide - antagonists & inhibitors Hydrogen Peroxide - pharmacology In Situ Nick-End Labeling Isoquinolines - pharmacology Medical sciences Myocardial apoptosis Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Oxidative Stress - drug effects PARP inhibitor Poly(ADP-ribose) Polymerase Inhibitors Poly(ADP-ribose) Polymerases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats Reactive oxygen species Reactive Oxygen Species - metabolism Signal Transduction - drug effects Toxicology |
| title | 5-AIQ inhibits H2O2-induced apoptosis through reactive oxygen species scavenging and Akt/GSK-3β signaling pathway in H9c2 cardiomyocytes |
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