Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN
This study is aimed to investigate the effect of pinoresinol diglucoside (PDG) in ameliorating myocardial ischemia–reperfusion injury (MIRI). Hypoxia/reperfusion (H/R)‐induced H9c2 cardiomyocytes were used to establish an in‐vitro ischemia–reperfusion injury model of cardiomyocytes. Cells were treat...
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Veröffentlicht in: | Journal of biochemical and molecular toxicology 2022-10, Vol.36 (10), p.e23175-n/a |
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description | This study is aimed to investigate the effect of pinoresinol diglucoside (PDG) in ameliorating myocardial ischemia–reperfusion injury (MIRI). Hypoxia/reperfusion (H/R)‐induced H9c2 cardiomyocytes were used to establish an in‐vitro ischemia–reperfusion injury model of cardiomyocytes. Cells were treated with 1 μmol/L of PDG. Reactive oxygen species (ROS) level was detected by a 2′,7′‐dichlorofluorescein‐diacetate assay. The release of lactate dehydrogenase (LDH) and creatine kinase‐MB (CK‐MB) was examined by enzyme‐linked immunosorbent assay. The viability and apoptosis of H9c2 cells were probed by MTT assay and flow cytometry. Besides this, Western blot and quantitative real‐time PCR were used to detect microRNA‐142‐3p (miR‐142‐3p) and hypoxia‐inducible factor 1 subunit alpha inhibitor (HIF1AN) expression levels. The binding sequence between miR‐142‐3p and HIF1AN 3′‐untranslated region was validated by a dual‐luciferase reporter gene assay. PDG treatment significantly reduced the level of ROS, LDH, and CK‐MB, promoted viability, and inhibited the apoptosis of H9c2 cells. PDG treatment promoted miR‐142‐3p expression and inhibited HIF1AN expression in H9c2 cells. MiR‐142‐3p overexpression enhanced the effects of PDG on ROS, LDH, CK‐MB levels, cell viability, and apoptosis in H9c2 cardiomyocytes, while overexpression of HIF1AN reversed the above effects. PDG ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN. |
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Hypoxia/reperfusion (H/R)‐induced H9c2 cardiomyocytes were used to establish an in‐vitro ischemia–reperfusion injury model of cardiomyocytes. Cells were treated with 1 μmol/L of PDG. Reactive oxygen species (ROS) level was detected by a 2′,7′‐dichlorofluorescein‐diacetate assay. The release of lactate dehydrogenase (LDH) and creatine kinase‐MB (CK‐MB) was examined by enzyme‐linked immunosorbent assay. The viability and apoptosis of H9c2 cells were probed by MTT assay and flow cytometry. Besides this, Western blot and quantitative real‐time PCR were used to detect microRNA‐142‐3p (miR‐142‐3p) and hypoxia‐inducible factor 1 subunit alpha inhibitor (HIF1AN) expression levels. The binding sequence between miR‐142‐3p and HIF1AN 3′‐untranslated region was validated by a dual‐luciferase reporter gene assay. PDG treatment significantly reduced the level of ROS, LDH, and CK‐MB, promoted viability, and inhibited the apoptosis of H9c2 cells. PDG treatment promoted miR‐142‐3p expression and inhibited HIF1AN expression in H9c2 cells. MiR‐142‐3p overexpression enhanced the effects of PDG on ROS, LDH, CK‐MB levels, cell viability, and apoptosis in H9c2 cardiomyocytes, while overexpression of HIF1AN reversed the above effects. PDG ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN.</description><identifier>ISSN: 1095-6670</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.23175</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc</publisher><subject>3' Untranslated regions ; Apoptosis ; Assaying ; Cardiomyocytes ; Cell viability ; Creatine ; Creatine kinase ; Flow cytometry ; HIF1AN ; Hypoxia ; Injuries ; Ischemia ; Kinases ; L-Lactate dehydrogenase ; Lactate dehydrogenase ; Lactic acid ; miRNA ; miR‐142‐3p ; Myocardial ischemia ; myocardial ischemia–reperfusion injury ; pinoresinol diglucoside ; Reactive oxygen species ; Reperfusion ; Reporter gene ; Ribonucleic acid ; RNA</subject><ispartof>Journal of biochemical and molecular toxicology, 2022-10, Vol.36 (10), p.e23175-n/a</ispartof><rights>2022 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2605-c270b0741a30779eee3252d4ce9fd38af388eadd11cee9fe06330e00f1009d6b3</citedby><cites>FETCH-LOGICAL-c2605-c270b0741a30779eee3252d4ce9fd38af388eadd11cee9fe06330e00f1009d6b3</cites><orcidid>0000-0002-3299-4797</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjbt.23175$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjbt.23175$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids></links><search><creatorcontrib>Wei, Yuan</creatorcontrib><creatorcontrib>Xiao, Liang</creatorcontrib><creatorcontrib>Yingying, Liu</creatorcontrib><creatorcontrib>Haichen, Wang</creatorcontrib><title>Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN</title><title>Journal of biochemical and molecular toxicology</title><description>This study is aimed to investigate the effect of pinoresinol diglucoside (PDG) in ameliorating myocardial ischemia–reperfusion injury (MIRI). Hypoxia/reperfusion (H/R)‐induced H9c2 cardiomyocytes were used to establish an in‐vitro ischemia–reperfusion injury model of cardiomyocytes. Cells were treated with 1 μmol/L of PDG. Reactive oxygen species (ROS) level was detected by a 2′,7′‐dichlorofluorescein‐diacetate assay. The release of lactate dehydrogenase (LDH) and creatine kinase‐MB (CK‐MB) was examined by enzyme‐linked immunosorbent assay. The viability and apoptosis of H9c2 cells were probed by MTT assay and flow cytometry. Besides this, Western blot and quantitative real‐time PCR were used to detect microRNA‐142‐3p (miR‐142‐3p) and hypoxia‐inducible factor 1 subunit alpha inhibitor (HIF1AN) expression levels. The binding sequence between miR‐142‐3p and HIF1AN 3′‐untranslated region was validated by a dual‐luciferase reporter gene assay. PDG treatment significantly reduced the level of ROS, LDH, and CK‐MB, promoted viability, and inhibited the apoptosis of H9c2 cells. PDG treatment promoted miR‐142‐3p expression and inhibited HIF1AN expression in H9c2 cells. MiR‐142‐3p overexpression enhanced the effects of PDG on ROS, LDH, CK‐MB levels, cell viability, and apoptosis in H9c2 cardiomyocytes, while overexpression of HIF1AN reversed the above effects. PDG ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN.</description><subject>3' Untranslated regions</subject><subject>Apoptosis</subject><subject>Assaying</subject><subject>Cardiomyocytes</subject><subject>Cell viability</subject><subject>Creatine</subject><subject>Creatine kinase</subject><subject>Flow cytometry</subject><subject>HIF1AN</subject><subject>Hypoxia</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>L-Lactate dehydrogenase</subject><subject>Lactate dehydrogenase</subject><subject>Lactic acid</subject><subject>miRNA</subject><subject>miR‐142‐3p</subject><subject>Myocardial ischemia</subject><subject>myocardial ischemia–reperfusion injury</subject><subject>pinoresinol diglucoside</subject><subject>Reactive oxygen species</subject><subject>Reperfusion</subject><subject>Reporter gene</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><issn>1095-6670</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp10M1KAzEUBeAgCtbqwjcIuNFF25uk87esYm2lqEhdD2lyp6TMTGoyg8zOR_AZfRLT1pXg5iSE717CIeSSwZAB8NFm1Qy5YEl0RHoMsmwA45gd7-_RII4TOCVn3m8AIMqSqEfci6mtQx-ypNqsy1ZZbzRSWWFprJMNejobvX5_fplatwo1NfWmdR21BVXSaWOrzqpux1YddbhuS9mYek0rsxtiYx5SbKmsNZ3Np2zydE5OCll6vPg9--Rter-8mw0Wzw_zu8lioHgMUcgEVpCMmRSQJBkiCh5xPVaYFVqkshBpilJrxhSGJ4RYCECAIvSQ6Xgl-uT6sHfr7HuLvskr4xWWpazRtj4P-zlLUsZEoFd_6Ma2rg6_C4qLCDK-VzcHpZz13mGRb52ppOtyBvmu_Ty0n-_bD3Z0sB-mxO5_mD_eLg8TP7kuiKA</recordid><startdate>202210</startdate><enddate>202210</enddate><creator>Wei, Yuan</creator><creator>Xiao, Liang</creator><creator>Yingying, Liu</creator><creator>Haichen, Wang</creator><general>Wiley Subscription Services, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3299-4797</orcidid></search><sort><creationdate>202210</creationdate><title>Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN</title><author>Wei, Yuan ; Xiao, Liang ; Yingying, Liu ; Haichen, Wang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2605-c270b0741a30779eee3252d4ce9fd38af388eadd11cee9fe06330e00f1009d6b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>3' Untranslated regions</topic><topic>Apoptosis</topic><topic>Assaying</topic><topic>Cardiomyocytes</topic><topic>Cell viability</topic><topic>Creatine</topic><topic>Creatine kinase</topic><topic>Flow cytometry</topic><topic>HIF1AN</topic><topic>Hypoxia</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>L-Lactate dehydrogenase</topic><topic>Lactate dehydrogenase</topic><topic>Lactic acid</topic><topic>miRNA</topic><topic>miR‐142‐3p</topic><topic>Myocardial ischemia</topic><topic>myocardial ischemia–reperfusion injury</topic><topic>pinoresinol diglucoside</topic><topic>Reactive oxygen species</topic><topic>Reperfusion</topic><topic>Reporter gene</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wei, Yuan</creatorcontrib><creatorcontrib>Xiao, Liang</creatorcontrib><creatorcontrib>Yingying, Liu</creatorcontrib><creatorcontrib>Haichen, Wang</creatorcontrib><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wei, Yuan</au><au>Xiao, Liang</au><au>Yingying, Liu</au><au>Haichen, Wang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><date>2022-10</date><risdate>2022</risdate><volume>36</volume><issue>10</issue><spage>e23175</spage><epage>n/a</epage><pages>e23175-n/a</pages><issn>1095-6670</issn><eissn>1099-0461</eissn><abstract>This study is aimed to investigate the effect of pinoresinol diglucoside (PDG) in ameliorating myocardial ischemia–reperfusion injury (MIRI). Hypoxia/reperfusion (H/R)‐induced H9c2 cardiomyocytes were used to establish an in‐vitro ischemia–reperfusion injury model of cardiomyocytes. Cells were treated with 1 μmol/L of PDG. Reactive oxygen species (ROS) level was detected by a 2′,7′‐dichlorofluorescein‐diacetate assay. The release of lactate dehydrogenase (LDH) and creatine kinase‐MB (CK‐MB) was examined by enzyme‐linked immunosorbent assay. The viability and apoptosis of H9c2 cells were probed by MTT assay and flow cytometry. Besides this, Western blot and quantitative real‐time PCR were used to detect microRNA‐142‐3p (miR‐142‐3p) and hypoxia‐inducible factor 1 subunit alpha inhibitor (HIF1AN) expression levels. The binding sequence between miR‐142‐3p and HIF1AN 3′‐untranslated region was validated by a dual‐luciferase reporter gene assay. PDG treatment significantly reduced the level of ROS, LDH, and CK‐MB, promoted viability, and inhibited the apoptosis of H9c2 cells. PDG treatment promoted miR‐142‐3p expression and inhibited HIF1AN expression in H9c2 cells. MiR‐142‐3p overexpression enhanced the effects of PDG on ROS, LDH, CK‐MB levels, cell viability, and apoptosis in H9c2 cardiomyocytes, while overexpression of HIF1AN reversed the above effects. PDG ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc</pub><doi>10.1002/jbt.23175</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-3299-4797</orcidid></addata></record> |
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subjects | 3' Untranslated regions Apoptosis Assaying Cardiomyocytes Cell viability Creatine Creatine kinase Flow cytometry HIF1AN Hypoxia Injuries Ischemia Kinases L-Lactate dehydrogenase Lactate dehydrogenase Lactic acid miRNA miR‐142‐3p Myocardial ischemia myocardial ischemia–reperfusion injury pinoresinol diglucoside Reactive oxygen species Reperfusion Reporter gene Ribonucleic acid RNA |
title | Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN |
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