Curcumin attenuates hypoxia/reoxygenation‑induced cardiomyocyte injury by downregulating Notch signaling
Recovery of the blood supply is the most effective treatment against ischemic heart disease; however, it is also a major cause of myocardial ischemia/reperfusion injury in clinical therapy. Curcumin has been reported to possess beneficial effects against hypoxia/reoxygenation (H/R)‑induced cardiomyo...
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| Veröffentlicht in: | Molecular medicine reports 2019-08, Vol.20 (2), p.1541-1550 |
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| creator | Zhu, Peng Yang, Manli He, Hao Kuang, Zhibin Liang, Mu Lin, Anxiao Liang, Song Wen, Qiyun Cheng, Zhiqin Sun, Chaofeng |
| description | Recovery of the blood supply is the most effective treatment against ischemic heart disease; however, it is also a major cause of myocardial ischemia/reperfusion injury in clinical therapy. Curcumin has been reported to possess beneficial effects against hypoxia/reoxygenation (H/R)‑induced cardiomyocyte injury by regulating cell proliferation, apoptosis and antioxidant enzyme activity. The aim of the present study was to investigate the molecular mechanisms underlying the effects of curcumin on H/R‑injured cardiomyocytes. H9C2 cardiomyocytes were pretreated with curcumin, and then cultured under H/R conditions. The viability of H9C2 cells was measured using a Cell Counting kit‑8 assay, and the levels of intracellular lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured to assess cell injury. Levels of reactive oxygen species (ROS) and apoptosis were evaluated by flow cytometry. The expression levels of Notch intracellular domain (NICD) and numerous downstream genes were analyzed via reverse transcription‑quantitative polymerase chain reaction and western blotting. The results revealed that curcumin protected H9C2 cells against H/R‑induced injury, reversing the H/R‑induced increases in LDH and MDA levels, and decreases in SOD levels. ROS levels in H/R‑induced cells were also significantly downregulated by curcumin treatment (P |
| doi_str_mv | 10.3892/mmr.2019.10371 |
| format | Article |
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Curcumin has been reported to possess beneficial effects against hypoxia/reoxygenation (H/R)‑induced cardiomyocyte injury by regulating cell proliferation, apoptosis and antioxidant enzyme activity. The aim of the present study was to investigate the molecular mechanisms underlying the effects of curcumin on H/R‑injured cardiomyocytes. H9C2 cardiomyocytes were pretreated with curcumin, and then cultured under H/R conditions. The viability of H9C2 cells was measured using a Cell Counting kit‑8 assay, and the levels of intracellular lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured to assess cell injury. Levels of reactive oxygen species (ROS) and apoptosis were evaluated by flow cytometry. The expression levels of Notch intracellular domain (NICD) and numerous downstream genes were analyzed via reverse transcription‑quantitative polymerase chain reaction and western blotting. The results revealed that curcumin protected H9C2 cells against H/R‑induced injury, reversing the H/R‑induced increases in LDH and MDA levels, and decreases in SOD levels. ROS levels in H/R‑induced cells were also significantly downregulated by curcumin treatment (P<0.01), and the apoptotic rate was significantly decreased from 15.13% in the H/R group to 7.7% in the H/R + curcumin group (P<0.01). The expression levels of NICD, hairy and enhancer of split (Hes)‑1, Hes‑5 and hairy/enhancer‑of‑split related with YRPW motif protein 1 (Hey‑1) were significantly decreased in H/R‑treated cells following curcumin treatment. Treatment with Jagged1 attenuated the effects of curcumin on cell viability, ROS levels and apoptosis; the Notch pathway was also reactivated. The present study indicated that there was a role for the Notch pathway in the protective effects of curcumin against H/R‑induced cardiomyocyte injury, suggesting that downregulation of the Notch pathway may alleviate H/R‑induced injury in H9C2 cells.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2019.10371</identifier><identifier>PMID: 31257466</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Analysis ; Animals ; Antioxidants ; Antioxidants (Nutrients) ; Antioxidants - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Cardiomyocytes ; Cardiovascular diseases ; Cell cycle ; Cell growth ; Cell Hypoxia ; Cell injury ; Cell Line ; Cell proliferation ; Cell Survival - drug effects ; Cell viability ; Coronary artery disease ; Curcumin ; Curcumin - pharmacology ; Dehydrogenases ; Enhancer-of-split protein ; Enzymatic activity ; Enzymes ; Flow cytometry ; Gene expression ; Gene Expression Regulation ; Genes ; Heart cells ; Heart diseases ; Hypotheses ; Hypoxia ; Intracellular ; Ischemia ; Jagged-1 Protein - pharmacology ; Jagged1 protein ; L-Lactate dehydrogenase ; L-Lactate Dehydrogenase - genetics ; L-Lactate Dehydrogenase - metabolism ; Lactic acid ; Ligands ; Malondialdehyde ; Malondialdehyde - antagonists & inhibitors ; Malondialdehyde - metabolism ; Mammals ; Molecular modelling ; Myocardial ischemia ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Oxygen - pharmacology ; Polymerase chain reaction ; Proteins ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - antagonists & inhibitors ; Reactive Oxygen Species - metabolism ; Receptors, Notch - antagonists & inhibitors ; Receptors, Notch - genetics ; Receptors, Notch - metabolism ; Reperfusion ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Reverse transcription ; Scientific equipment industry ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Studies ; Superoxide dismutase ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism ; Superoxides ; Transcription (Genetics) ; Transcription Factor HES-1 - genetics ; Transcription Factor HES-1 - metabolism ; Western blotting</subject><ispartof>Molecular medicine reports, 2019-08, Vol.20 (2), p.1541-1550</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Zhu et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-54b7cc875be59e15ae18bec27c96e6505ca5e2820c17cd976723bcb02a67ea373</citedby><cites>FETCH-LOGICAL-c485t-54b7cc875be59e15ae18bec27c96e6505ca5e2820c17cd976723bcb02a67ea373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31257466$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Peng</creatorcontrib><creatorcontrib>Yang, Manli</creatorcontrib><creatorcontrib>He, Hao</creatorcontrib><creatorcontrib>Kuang, Zhibin</creatorcontrib><creatorcontrib>Liang, Mu</creatorcontrib><creatorcontrib>Lin, Anxiao</creatorcontrib><creatorcontrib>Liang, Song</creatorcontrib><creatorcontrib>Wen, Qiyun</creatorcontrib><creatorcontrib>Cheng, Zhiqin</creatorcontrib><creatorcontrib>Sun, Chaofeng</creatorcontrib><title>Curcumin attenuates hypoxia/reoxygenation‑induced cardiomyocyte injury by downregulating Notch signaling</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Recovery of the blood supply is the most effective treatment against ischemic heart disease; however, it is also a major cause of myocardial ischemia/reperfusion injury in clinical therapy. Curcumin has been reported to possess beneficial effects against hypoxia/reoxygenation (H/R)‑induced cardiomyocyte injury by regulating cell proliferation, apoptosis and antioxidant enzyme activity. The aim of the present study was to investigate the molecular mechanisms underlying the effects of curcumin on H/R‑injured cardiomyocytes. H9C2 cardiomyocytes were pretreated with curcumin, and then cultured under H/R conditions. The viability of H9C2 cells was measured using a Cell Counting kit‑8 assay, and the levels of intracellular lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured to assess cell injury. Levels of reactive oxygen species (ROS) and apoptosis were evaluated by flow cytometry. The expression levels of Notch intracellular domain (NICD) and numerous downstream genes were analyzed via reverse transcription‑quantitative polymerase chain reaction and western blotting. The results revealed that curcumin protected H9C2 cells against H/R‑induced injury, reversing the H/R‑induced increases in LDH and MDA levels, and decreases in SOD levels. ROS levels in H/R‑induced cells were also significantly downregulated by curcumin treatment (P<0.01), and the apoptotic rate was significantly decreased from 15.13% in the H/R group to 7.7% in the H/R + curcumin group (P<0.01). The expression levels of NICD, hairy and enhancer of split (Hes)‑1, Hes‑5 and hairy/enhancer‑of‑split related with YRPW motif protein 1 (Hey‑1) were significantly decreased in H/R‑treated cells following curcumin treatment. Treatment with Jagged1 attenuated the effects of curcumin on cell viability, ROS levels and apoptosis; the Notch pathway was also reactivated. The present study indicated that there was a role for the Notch pathway in the protective effects of curcumin against H/R‑induced cardiomyocyte injury, suggesting that downregulation of the Notch pathway may alleviate H/R‑induced injury in H9C2 cells.</description><subject>Analysis</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants (Nutrients)</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular diseases</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Hypoxia</subject><subject>Cell injury</subject><subject>Cell Line</subject><subject>Cell proliferation</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Coronary artery disease</subject><subject>Curcumin</subject><subject>Curcumin - pharmacology</subject><subject>Dehydrogenases</subject><subject>Enhancer-of-split protein</subject><subject>Enzymatic activity</subject><subject>Enzymes</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Heart cells</subject><subject>Heart diseases</subject><subject>Hypotheses</subject><subject>Hypoxia</subject><subject>Intracellular</subject><subject>Ischemia</subject><subject>Jagged-1 Protein - pharmacology</subject><subject>Jagged1 protein</subject><subject>L-Lactate dehydrogenase</subject><subject>L-Lactate Dehydrogenase - genetics</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Lactic acid</subject><subject>Ligands</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - antagonists & inhibitors</subject><subject>Malondialdehyde - metabolism</subject><subject>Mammals</subject><subject>Molecular modelling</subject><subject>Myocardial ischemia</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Oxygen - pharmacology</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Rats</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - antagonists & inhibitors</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, Notch - antagonists & inhibitors</subject><subject>Receptors, Notch - genetics</subject><subject>Receptors, Notch - metabolism</subject><subject>Reperfusion</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Reverse transcription</subject><subject>Scientific equipment industry</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Studies</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxides</subject><subject>Transcription (Genetics)</subject><subject>Transcription Factor HES-1 - genetics</subject><subject>Transcription Factor HES-1 - metabolism</subject><subject>Western blotting</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkstu1DAUhiNERUthyxJFYtPNTH2JbxukatQCUlU2sLYc50zGo8Qe7BiaHa_AK_ZJ8JShXFR5cezj7_-tY_1V9QqjJZWKnI9jXBKE1RIjKvCT6gQLhRcUoebpYU-UEsfV85S2CHFGmHpWHVNMmGg4P6m2qxxtHp2vzTSBz2aCVG_mXbh15jxCuJ178GZywd99_-F8ly10tTWxc2Gcg50nqJ3f5jjX7Vx34ZuP0OehCHxf34TJburkem-Gcn5RHa3NkODloZ5Wn68uP63eL64_vvuwurhe2EayacGaVlgrBWuBKcDMAJYtWCKs4sAZYtYwIJIgi4XtlOCC0Na2iBguwFBBT6u3v3x3uR2hs-CnaAa9i240cdbBOP3vjXcb3YevmnPCGoSKwdnBIIYvGdKkR5csDIPxEHLShDDECaXNHn3zH7oNOZZ57ynJaKMa_ofqzQDa-XUo79q9qb5gSkgmhZSFWj5CldXB6GzwsHal_5jAxpBShPXDjBjpfTp0SYfep0Pfp6MIXv_9Mw_47zjQn0YPuTk</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Zhu, Peng</creator><creator>Yang, Manli</creator><creator>He, Hao</creator><creator>Kuang, Zhibin</creator><creator>Liang, Mu</creator><creator>Lin, Anxiao</creator><creator>Liang, Song</creator><creator>Wen, Qiyun</creator><creator>Cheng, Zhiqin</creator><creator>Sun, Chaofeng</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190801</creationdate><title>Curcumin attenuates hypoxia/reoxygenation‑induced cardiomyocyte injury by downregulating Notch signaling</title><author>Zhu, Peng ; Yang, Manli ; He, Hao ; Kuang, Zhibin ; Liang, Mu ; Lin, Anxiao ; Liang, Song ; Wen, Qiyun ; Cheng, Zhiqin ; Sun, Chaofeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-54b7cc875be59e15ae18bec27c96e6505ca5e2820c17cd976723bcb02a67ea373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants (Nutrients)</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular diseases</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Hypoxia</topic><topic>Cell injury</topic><topic>Cell Line</topic><topic>Cell proliferation</topic><topic>Cell Survival - drug effects</topic><topic>Cell viability</topic><topic>Coronary artery disease</topic><topic>Curcumin</topic><topic>Curcumin - pharmacology</topic><topic>Dehydrogenases</topic><topic>Enhancer-of-split protein</topic><topic>Enzymatic activity</topic><topic>Enzymes</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Genes</topic><topic>Heart cells</topic><topic>Heart diseases</topic><topic>Hypotheses</topic><topic>Hypoxia</topic><topic>Intracellular</topic><topic>Ischemia</topic><topic>Jagged-1 Protein - pharmacology</topic><topic>Jagged1 protein</topic><topic>L-Lactate dehydrogenase</topic><topic>L-Lactate Dehydrogenase - genetics</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Lactic acid</topic><topic>Ligands</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - antagonists & inhibitors</topic><topic>Malondialdehyde - metabolism</topic><topic>Mammals</topic><topic>Molecular modelling</topic><topic>Myocardial ischemia</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Oxygen - pharmacology</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - antagonists & inhibitors</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors, Notch - antagonists & inhibitors</topic><topic>Receptors, Notch - genetics</topic><topic>Receptors, Notch - metabolism</topic><topic>Reperfusion</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>Reverse transcription</topic><topic>Scientific equipment industry</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>Studies</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Superoxides</topic><topic>Transcription (Genetics)</topic><topic>Transcription Factor HES-1 - genetics</topic><topic>Transcription Factor HES-1 - metabolism</topic><topic>Western blotting</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Peng</creatorcontrib><creatorcontrib>Yang, Manli</creatorcontrib><creatorcontrib>He, Hao</creatorcontrib><creatorcontrib>Kuang, Zhibin</creatorcontrib><creatorcontrib>Liang, Mu</creatorcontrib><creatorcontrib>Lin, Anxiao</creatorcontrib><creatorcontrib>Liang, Song</creatorcontrib><creatorcontrib>Wen, Qiyun</creatorcontrib><creatorcontrib>Cheng, Zhiqin</creatorcontrib><creatorcontrib>Sun, Chaofeng</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 & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological 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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Peng</au><au>Yang, Manli</au><au>He, Hao</au><au>Kuang, Zhibin</au><au>Liang, Mu</au><au>Lin, Anxiao</au><au>Liang, Song</au><au>Wen, Qiyun</au><au>Cheng, Zhiqin</au><au>Sun, Chaofeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Curcumin attenuates hypoxia/reoxygenation‑induced cardiomyocyte injury by downregulating Notch signaling</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>20</volume><issue>2</issue><spage>1541</spage><epage>1550</epage><pages>1541-1550</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Recovery of the blood supply is the most effective treatment against ischemic heart disease; however, it is also a major cause of myocardial ischemia/reperfusion injury in clinical therapy. Curcumin has been reported to possess beneficial effects against hypoxia/reoxygenation (H/R)‑induced cardiomyocyte injury by regulating cell proliferation, apoptosis and antioxidant enzyme activity. The aim of the present study was to investigate the molecular mechanisms underlying the effects of curcumin on H/R‑injured cardiomyocytes. H9C2 cardiomyocytes were pretreated with curcumin, and then cultured under H/R conditions. The viability of H9C2 cells was measured using a Cell Counting kit‑8 assay, and the levels of intracellular lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured to assess cell injury. Levels of reactive oxygen species (ROS) and apoptosis were evaluated by flow cytometry. The expression levels of Notch intracellular domain (NICD) and numerous downstream genes were analyzed via reverse transcription‑quantitative polymerase chain reaction and western blotting. The results revealed that curcumin protected H9C2 cells against H/R‑induced injury, reversing the H/R‑induced increases in LDH and MDA levels, and decreases in SOD levels. ROS levels in H/R‑induced cells were also significantly downregulated by curcumin treatment (P<0.01), and the apoptotic rate was significantly decreased from 15.13% in the H/R group to 7.7% in the H/R + curcumin group (P<0.01). The expression levels of NICD, hairy and enhancer of split (Hes)‑1, Hes‑5 and hairy/enhancer‑of‑split related with YRPW motif protein 1 (Hey‑1) were significantly decreased in H/R‑treated cells following curcumin treatment. Treatment with Jagged1 attenuated the effects of curcumin on cell viability, ROS levels and apoptosis; the Notch pathway was also reactivated. The present study indicated that there was a role for the Notch pathway in the protective effects of curcumin against H/R‑induced cardiomyocyte injury, suggesting that downregulation of the Notch pathway may alleviate H/R‑induced injury in H9C2 cells.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>31257466</pmid><doi>10.3892/mmr.2019.10371</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular medicine reports, 2019-08, Vol.20 (2), p.1541-1550 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Analysis Animals Antioxidants Antioxidants (Nutrients) Antioxidants - pharmacology Apoptosis Apoptosis - drug effects Apoptosis - genetics Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Cardiomyocytes Cardiovascular diseases Cell cycle Cell growth Cell Hypoxia Cell injury Cell Line Cell proliferation Cell Survival - drug effects Cell viability Coronary artery disease Curcumin Curcumin - pharmacology Dehydrogenases Enhancer-of-split protein Enzymatic activity Enzymes Flow cytometry Gene expression Gene Expression Regulation Genes Heart cells Heart diseases Hypotheses Hypoxia Intracellular Ischemia Jagged-1 Protein - pharmacology Jagged1 protein L-Lactate dehydrogenase L-Lactate Dehydrogenase - genetics L-Lactate Dehydrogenase - metabolism Lactic acid Ligands Malondialdehyde Malondialdehyde - antagonists & inhibitors Malondialdehyde - metabolism Mammals Molecular modelling Myocardial ischemia Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Oxygen - pharmacology Polymerase chain reaction Proteins Rats Reactive oxygen species Reactive Oxygen Species - antagonists & inhibitors Reactive Oxygen Species - metabolism Receptors, Notch - antagonists & inhibitors Receptors, Notch - genetics Receptors, Notch - metabolism Reperfusion Repressor Proteins - genetics Repressor Proteins - metabolism Reverse transcription Scientific equipment industry Signal Transduction - drug effects Signal Transduction - genetics Studies Superoxide dismutase Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Superoxides Transcription (Genetics) Transcription Factor HES-1 - genetics Transcription Factor HES-1 - metabolism Western blotting |
| title | Curcumin attenuates hypoxia/reoxygenation‑induced cardiomyocyte injury by downregulating Notch signaling |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-11T18%3A45%3A05IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Curcumin%20attenuates%20hypoxia/reoxygenation%E2%80%91induced%20cardiomyocyte%20injury%20by%20downregulating%20Notch%20signaling&rft.jtitle=Molecular%20medicine%20reports&rft.au=Zhu,%20Peng&rft.date=2019-08-01&rft.volume=20&rft.issue=2&rft.spage=1541&rft.epage=1550&rft.pages=1541-1550&rft.issn=1791-2997&rft.eissn=1791-3004&rft_id=info:doi/10.3892/mmr.2019.10371&rft_dat=%3Cgale_pubme%3EA597858788%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2258534946&rft_id=info:pmid/31257466&rft_galeid=A597858788&rfr_iscdi=true |