Vanillic Acid Alleviates Acute Myocardial Hypoxia/Reoxygenation Injury by Inhibiting Oxidative Stress
Oxidative stress is an important factor of myocardial hypoxia/reoxygenation (H/R) injury. Our research focuses on how to reduce the cardiac toxicity caused by oxidative stress through natural plant extracts. Vanillic acid (VA) is a phenolic compound found in edible plants and rich in the roots of An...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2020, Vol.2020 (2020), p.1-12 |
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| creator | Yi, Bo Hu, Wenfeng Qin, Mingming Jiao, Shoufeng Yao, Xiuya Liu, Dan |
| description | Oxidative stress is an important factor of myocardial hypoxia/reoxygenation (H/R) injury. Our research focuses on how to reduce the cardiac toxicity caused by oxidative stress through natural plant extracts. Vanillic acid (VA) is a phenolic compound found in edible plants and rich in the roots of Angelica sinensis. Experimental studies have provided evidence for this compound’s effectiveness in cardiovascular diseases; however, its mechanism is still unclear. In this study, molecular mechanisms related to the protective effects of VA were investigated in H9c2 cells in the context of H/R injury. The results showed that pretreatment with VA significantly increased cell viability and decreased the percentage of apoptotic cells, as well as lactate dehydrogenase and creatine phosphokinase activity, in the supernatant, accompanied by reduced levels of reactive oxygen species and reduced caspase-3 activity. VA pretreatment also restored mitochondrial membrane potentials. Moreover, preincubation with VA significantly attenuated mitochondrial permeability transition pore activity. VA administration upregulated adenosine monophosphate-activated protein kinase α2 (AMPKα2) protein expression, and interestingly, pretreatment with AMPKα2-siRNA lentivirus effectively attenuated the cardioprotective effects of VA in response to H/R injury. |
| doi_str_mv | 10.1155/2020/8348035 |
| format | Article |
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Our research focuses on how to reduce the cardiac toxicity caused by oxidative stress through natural plant extracts. Vanillic acid (VA) is a phenolic compound found in edible plants and rich in the roots of Angelica sinensis. Experimental studies have provided evidence for this compound’s effectiveness in cardiovascular diseases; however, its mechanism is still unclear. In this study, molecular mechanisms related to the protective effects of VA were investigated in H9c2 cells in the context of H/R injury. The results showed that pretreatment with VA significantly increased cell viability and decreased the percentage of apoptotic cells, as well as lactate dehydrogenase and creatine phosphokinase activity, in the supernatant, accompanied by reduced levels of reactive oxygen species and reduced caspase-3 activity. VA pretreatment also restored mitochondrial membrane potentials. Moreover, preincubation with VA significantly attenuated mitochondrial permeability transition pore activity. VA administration upregulated adenosine monophosphate-activated protein kinase α2 (AMPKα2) protein expression, and interestingly, pretreatment with AMPKα2-siRNA lentivirus effectively attenuated the cardioprotective effects of VA in response to H/R injury.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2020/8348035</identifier><identifier>PMID: 32377308</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Apoptosis ; Biological products ; Cell Hypoxia - drug effects ; Creatine kinase ; Flow cytometry ; Fluorides ; Humans ; Hypoxia ; Kinases ; Membranes ; Mitochondria ; Myocardial Reperfusion Injury - drug therapy ; Oxidative Stress ; Protein kinases ; Proteins ; Rats ; Reactive Oxygen Species ; Vanillic Acid - therapeutic use</subject><ispartof>Oxidative medicine and cellular longevity, 2020, Vol.2020 (2020), p.1-12</ispartof><rights>Copyright © 2020 Xiuya Yao et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Xiuya Yao et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Xiuya Yao et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-5c7ce7a599212e71bb40226c108cb3947b26b694573806fda647851f4b1f419b3</citedby><cites>FETCH-LOGICAL-c499t-5c7ce7a599212e71bb40226c108cb3947b26b694573806fda647851f4b1f419b3</cites><orcidid>0000-0002-4684-0318 ; 0000-0002-7273-6741</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191373/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191373/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32377308$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Kibel, Aleksandar</contributor><contributor>Aleksandar Kibel</contributor><creatorcontrib>Yi, Bo</creatorcontrib><creatorcontrib>Hu, Wenfeng</creatorcontrib><creatorcontrib>Qin, Mingming</creatorcontrib><creatorcontrib>Jiao, Shoufeng</creatorcontrib><creatorcontrib>Yao, Xiuya</creatorcontrib><creatorcontrib>Liu, Dan</creatorcontrib><title>Vanillic Acid Alleviates Acute Myocardial Hypoxia/Reoxygenation Injury by Inhibiting Oxidative Stress</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Oxidative stress is an important factor of myocardial hypoxia/reoxygenation (H/R) injury. Our research focuses on how to reduce the cardiac toxicity caused by oxidative stress through natural plant extracts. Vanillic acid (VA) is a phenolic compound found in edible plants and rich in the roots of Angelica sinensis. Experimental studies have provided evidence for this compound’s effectiveness in cardiovascular diseases; however, its mechanism is still unclear. In this study, molecular mechanisms related to the protective effects of VA were investigated in H9c2 cells in the context of H/R injury. The results showed that pretreatment with VA significantly increased cell viability and decreased the percentage of apoptotic cells, as well as lactate dehydrogenase and creatine phosphokinase activity, in the supernatant, accompanied by reduced levels of reactive oxygen species and reduced caspase-3 activity. VA pretreatment also restored mitochondrial membrane potentials. Moreover, preincubation with VA significantly attenuated mitochondrial permeability transition pore activity. VA administration upregulated adenosine monophosphate-activated protein kinase α2 (AMPKα2) protein expression, and interestingly, pretreatment with AMPKα2-siRNA lentivirus effectively attenuated the cardioprotective effects of VA in response to H/R injury.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological products</subject><subject>Cell Hypoxia - drug effects</subject><subject>Creatine kinase</subject><subject>Flow cytometry</subject><subject>Fluorides</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Kinases</subject><subject>Membranes</subject><subject>Mitochondria</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Oxidative Stress</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Rats</subject><subject>Reactive Oxygen Species</subject><subject>Vanillic Acid - therapeutic use</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><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>eNqNkctrGzEQh5fS0jzaW89loZdA41qvXa0uBRPaJpAS6OsqJO2sLSNLrrTreP_7yNhx2p56EBoxH99o-BXFG4w-YFxVU4IImjaUNYhWz4pTLBiZICHY82ON0ElxltISoZoShl8WJ5RQzilqTgv4pbx1zppyZmxbzpyDjVU9pPweeii_jsGo2FrlyutxHbZWTb9B2I5z8Kq3wZc3fjnEsdRjrhZW2976eXm3tW1ub6D83kdI6VXxolMuwevDfV78_Pzpx9X15Pbuy83V7HZimBD9pDLcAFeVEAQT4FhrhgipDUaN0VQwrkmta8EqThtUd62qGW8q3DGdDxaanhcf9971oFfQGvB9VE6uo12pOMqgrPy74-1CzsNGciww5TQLLg6CGH4PkHq5ssmAc8pDGJIkVIiGsZo0GX33D7oMQ_R5vR3FmSAE10_UXDmQ1nchzzU7qZxlC-ac1CxTl3vKxJBShO74ZYzkLmW5S1keUs742z_XPMKPsWbg_R5YWN-qe_ufOsgMdOqJJqiqGkIfAH53uBk</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Yi, Bo</creator><creator>Hu, Wenfeng</creator><creator>Qin, Mingming</creator><creator>Jiao, Shoufeng</creator><creator>Yao, Xiuya</creator><creator>Liu, Dan</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4684-0318</orcidid><orcidid>https://orcid.org/0000-0002-7273-6741</orcidid></search><sort><creationdate>2020</creationdate><title>Vanillic Acid Alleviates Acute Myocardial Hypoxia/Reoxygenation Injury by Inhibiting Oxidative Stress</title><author>Yi, Bo ; Hu, Wenfeng ; Qin, Mingming ; Jiao, Shoufeng ; Yao, Xiuya ; Liu, Dan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-5c7ce7a599212e71bb40226c108cb3947b26b694573806fda647851f4b1f419b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological products</topic><topic>Cell Hypoxia - drug effects</topic><topic>Creatine kinase</topic><topic>Flow cytometry</topic><topic>Fluorides</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Kinases</topic><topic>Membranes</topic><topic>Mitochondria</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Oxidative Stress</topic><topic>Protein kinases</topic><topic>Proteins</topic><topic>Rats</topic><topic>Reactive Oxygen Species</topic><topic>Vanillic Acid - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yi, Bo</creatorcontrib><creatorcontrib>Hu, Wenfeng</creatorcontrib><creatorcontrib>Qin, Mingming</creatorcontrib><creatorcontrib>Jiao, Shoufeng</creatorcontrib><creatorcontrib>Yao, Xiuya</creatorcontrib><creatorcontrib>Liu, Dan</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><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>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>ProQuest Central Essentials</collection><collection>ProQuest Central</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yi, Bo</au><au>Hu, Wenfeng</au><au>Qin, Mingming</au><au>Jiao, Shoufeng</au><au>Yao, Xiuya</au><au>Liu, Dan</au><au>Kibel, Aleksandar</au><au>Aleksandar Kibel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vanillic Acid Alleviates Acute Myocardial Hypoxia/Reoxygenation Injury by Inhibiting Oxidative Stress</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2020</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>12</epage><pages>1-12</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Oxidative stress is an important factor of myocardial hypoxia/reoxygenation (H/R) injury. Our research focuses on how to reduce the cardiac toxicity caused by oxidative stress through natural plant extracts. Vanillic acid (VA) is a phenolic compound found in edible plants and rich in the roots of Angelica sinensis. Experimental studies have provided evidence for this compound’s effectiveness in cardiovascular diseases; however, its mechanism is still unclear. In this study, molecular mechanisms related to the protective effects of VA were investigated in H9c2 cells in the context of H/R injury. The results showed that pretreatment with VA significantly increased cell viability and decreased the percentage of apoptotic cells, as well as lactate dehydrogenase and creatine phosphokinase activity, in the supernatant, accompanied by reduced levels of reactive oxygen species and reduced caspase-3 activity. VA pretreatment also restored mitochondrial membrane potentials. Moreover, preincubation with VA significantly attenuated mitochondrial permeability transition pore activity. VA administration upregulated adenosine monophosphate-activated protein kinase α2 (AMPKα2) protein expression, and interestingly, pretreatment with AMPKα2-siRNA lentivirus effectively attenuated the cardioprotective effects of VA in response to H/R injury.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32377308</pmid><doi>10.1155/2020/8348035</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-4684-0318</orcidid><orcidid>https://orcid.org/0000-0002-7273-6741</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Biological products Cell Hypoxia - drug effects Creatine kinase Flow cytometry Fluorides Humans Hypoxia Kinases Membranes Mitochondria Myocardial Reperfusion Injury - drug therapy Oxidative Stress Protein kinases Proteins Rats Reactive Oxygen Species Vanillic Acid - therapeutic use |
| title | Vanillic Acid Alleviates Acute Myocardial Hypoxia/Reoxygenation Injury by Inhibiting Oxidative Stress |
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