Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats
Aim： Sevoflurane postconditioning （SpostC） has been shown to protect the heart from ischemia-reperfusion （I/R） injury. In this study, we examined whether SpostC affected autophagic flux in myocardial tissues that contributed to its cardioprotective effects in rats following acute I/R injury. Methods...
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| Veröffentlicht in: | Acta pharmacologica Sinica 2014-06, Vol.35 (6), p.758-769 |
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| container_title | Acta pharmacologica Sinica |
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| creator | Zhang, Yu-lin Yao, Yun-tai Fang, Neng-xin Zhou, Cheng-hui Gong, Jun-song Li, Li-huan |
| description | Aim： Sevoflurane postconditioning （SpostC） has been shown to protect the heart from ischemia-reperfusion （I/R） injury. In this study, we examined whether SpostC affected autophagic flux in myocardial tissues that contributed to its cardioprotective effects in rats following acute I/R injury.
Methods： SD rats underwent 30 min of left anterior descending coronary artery ligation followed by 120 min of reperfusion. The rats were subjected to inhalation of 2.4% （v/v） sevoflurane during the first 5 min of reperfusion, and chloroquine （10 mg/kg, ip） was injected 1 h before I/R. Myocardial infarct size was estimated using TTC staining. Autophagosomes in myocardial tissues were detected under TEM. Expression of LC3B-II, beclin-1, p62/SQSTM1, cathepsin B, caspase-3 and cleaved PARP was assessed using Western blot analysis. Plasma cardiac troponin I was measured using ELISA. Cardiomyocyte apoptosis was evaluated with TUNEL staining.
Results： I/R procedure produced severe myocardium infarct and apoptosis accompanied by markedly increased number of autophagosomes, as well as increased levels of LC3B-II, beclin-1 and p62 in myocardial tissues. SpostC significantly reduced infarct size, attenuated myocardial apoptosis, restored intact autophagic flux and improved the lysosomal function in myocardial tissues. Administration of chloroquine that blocked autophagic flux abrogated the cardioprotective effects of SpostC.
Conclusion： SpostC exerts its cardioprotective effects in rats following I/R injury via restoring autophagic flux in myocardial tissues. |
| doi_str_mv | 10.1038/aps.2014.20 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4086393</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>50237939</cqvip_id><sourcerecordid>3328492931</sourcerecordid><originalsourceid>FETCH-LOGICAL-c538t-6e9b5eac325d9b28d281af3a7c759de5094ce6c66092ab147db802dd57c8b27b3</originalsourceid><addsrcrecordid>eNptkc1rFDEYxoMotq6evEvEi6BT8zGZzFwEKX5BQRA9h0ySmU2ZTWaTTLGH_u99t7tdqnhJAs8vz_vxIPSSkjNKePtBz_mMEVrD8QidUlmLSjJRP4Z3I2lVk5afoGc5XxLCGafdU3TCatlxTrpTdPPT5RKTLj4GHAeslxLntR69wcO0_ME-4M11NDpZrydcfM6Ly9hnnNx28clZPMSE7_Q4p1icuXfK7iqCRdLB4TnmYmKwfif6MO5soWZ-jp4MesruxeFeod9fPv86_1Zd_Pj6_fzTRWUEb0vVuK4XThvOhO161lrWUj1wLY0UnXWCdLVxjWka0jHd01raviXMWiFN2zPZ8xX6uPedl37jrHGhJD2pOfmNTtcqaq_-VoJfqzFeKVhew2FVK_T2YJDiFjZQ1MZn46YJpotLVlTwGroQnAL65h_0Mi4pwHh3FKWUkBqod3vKpJhzcsOxGUrULlYFsapdrHAA_eph_0f2PkcA3u-BDFIYXXpQ9L9-rw_V1zGMW_hxtBSEcTDt-C2hpbwN</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1534111004</pqid></control><display><type>article</type><title>Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats</title><source>MEDLINE</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Zhang, Yu-lin ; Yao, Yun-tai ; Fang, Neng-xin ; Zhou, Cheng-hui ; Gong, Jun-song ; Li, Li-huan</creator><creatorcontrib>Zhang, Yu-lin ; Yao, Yun-tai ; Fang, Neng-xin ; Zhou, Cheng-hui ; Gong, Jun-song ; Li, Li-huan</creatorcontrib><description>Aim： Sevoflurane postconditioning （SpostC） has been shown to protect the heart from ischemia-reperfusion （I/R） injury. In this study, we examined whether SpostC affected autophagic flux in myocardial tissues that contributed to its cardioprotective effects in rats following acute I/R injury.
Methods： SD rats underwent 30 min of left anterior descending coronary artery ligation followed by 120 min of reperfusion. The rats were subjected to inhalation of 2.4% （v/v） sevoflurane during the first 5 min of reperfusion, and chloroquine （10 mg/kg, ip） was injected 1 h before I/R. Myocardial infarct size was estimated using TTC staining. Autophagosomes in myocardial tissues were detected under TEM. Expression of LC3B-II, beclin-1, p62/SQSTM1, cathepsin B, caspase-3 and cleaved PARP was assessed using Western blot analysis. Plasma cardiac troponin I was measured using ELISA. Cardiomyocyte apoptosis was evaluated with TUNEL staining.
Results： I/R procedure produced severe myocardium infarct and apoptosis accompanied by markedly increased number of autophagosomes, as well as increased levels of LC3B-II, beclin-1 and p62 in myocardial tissues. SpostC significantly reduced infarct size, attenuated myocardial apoptosis, restored intact autophagic flux and improved the lysosomal function in myocardial tissues. Administration of chloroquine that blocked autophagic flux abrogated the cardioprotective effects of SpostC.
Conclusion： SpostC exerts its cardioprotective effects in rats following I/R injury via restoring autophagic flux in myocardial tissues.</description><identifier>ISSN: 1671-4083</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1038/aps.2014.20</identifier><identifier>PMID: 24793309</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Anesthetics, Inhalation - therapeutic use ; Animals ; Autophagy - drug effects ; Biomedical and Life Sciences ; Biomedicine ; Cardiotonic Agents - therapeutic use ; Heart - drug effects ; Immunology ; Internal Medicine ; Male ; Medical Microbiology ; Methyl Ethers - therapeutic use ; Myocardial Infarction - drug therapy ; Myocardial Infarction - etiology ; Myocardial Infarction - pathology ; Myocardial Reperfusion Injury - complications ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - pathology ; Myocardium - pathology ; Original ; original-article ; Pharmacology/Toxicology ; Rats, Sprague-Dawley ; SD大鼠 ; Vaccine ; Western印迹 ; 七氟醚 ; 后处理 ; 心肌组织 ; 心脏 ; 自噬基因 ; 通量</subject><ispartof>Acta pharmacologica Sinica, 2014-06, Vol.35 (6), p.758-769</ispartof><rights>CPS and SIMM 2014</rights><rights>Copyright Nature Publishing Group Jun 2014</rights><rights>Copyright © 2014 CPS and SIMM 2014 CPS and SIMM</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-6e9b5eac325d9b28d281af3a7c759de5094ce6c66092ab147db802dd57c8b27b3</citedby><cites>FETCH-LOGICAL-c538t-6e9b5eac325d9b28d281af3a7c759de5094ce6c66092ab147db802dd57c8b27b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/95561A/95561A.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4086393/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4086393/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24793309$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yu-lin</creatorcontrib><creatorcontrib>Yao, Yun-tai</creatorcontrib><creatorcontrib>Fang, Neng-xin</creatorcontrib><creatorcontrib>Zhou, Cheng-hui</creatorcontrib><creatorcontrib>Gong, Jun-song</creatorcontrib><creatorcontrib>Li, Li-huan</creatorcontrib><title>Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacol Sin</addtitle><addtitle>Acta Pharmacologica Sinica</addtitle><description>Aim： Sevoflurane postconditioning （SpostC） has been shown to protect the heart from ischemia-reperfusion （I/R） injury. In this study, we examined whether SpostC affected autophagic flux in myocardial tissues that contributed to its cardioprotective effects in rats following acute I/R injury.
Methods： SD rats underwent 30 min of left anterior descending coronary artery ligation followed by 120 min of reperfusion. The rats were subjected to inhalation of 2.4% （v/v） sevoflurane during the first 5 min of reperfusion, and chloroquine （10 mg/kg, ip） was injected 1 h before I/R. Myocardial infarct size was estimated using TTC staining. Autophagosomes in myocardial tissues were detected under TEM. Expression of LC3B-II, beclin-1, p62/SQSTM1, cathepsin B, caspase-3 and cleaved PARP was assessed using Western blot analysis. Plasma cardiac troponin I was measured using ELISA. Cardiomyocyte apoptosis was evaluated with TUNEL staining.
Results： I/R procedure produced severe myocardium infarct and apoptosis accompanied by markedly increased number of autophagosomes, as well as increased levels of LC3B-II, beclin-1 and p62 in myocardial tissues. SpostC significantly reduced infarct size, attenuated myocardial apoptosis, restored intact autophagic flux and improved the lysosomal function in myocardial tissues. Administration of chloroquine that blocked autophagic flux abrogated the cardioprotective effects of SpostC.
Conclusion： SpostC exerts its cardioprotective effects in rats following I/R injury via restoring autophagic flux in myocardial tissues.</description><subject>Anesthetics, Inhalation - therapeutic use</subject><subject>Animals</subject><subject>Autophagy - drug effects</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cardiotonic Agents - therapeutic use</subject><subject>Heart - drug effects</subject><subject>Immunology</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medical Microbiology</subject><subject>Methyl Ethers - therapeutic use</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - etiology</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Reperfusion Injury - complications</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardium - pathology</subject><subject>Original</subject><subject>original-article</subject><subject>Pharmacology/Toxicology</subject><subject>Rats, Sprague-Dawley</subject><subject>SD大鼠</subject><subject>Vaccine</subject><subject>Western印迹</subject><subject>七氟醚</subject><subject>后处理</subject><subject>心肌组织</subject><subject>心脏</subject><subject>自噬基因</subject><subject>通量</subject><issn>1671-4083</issn><issn>1745-7254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkc1rFDEYxoMotq6evEvEi6BT8zGZzFwEKX5BQRA9h0ySmU2ZTWaTTLGH_u99t7tdqnhJAs8vz_vxIPSSkjNKePtBz_mMEVrD8QidUlmLSjJRP4Z3I2lVk5afoGc5XxLCGafdU3TCatlxTrpTdPPT5RKTLj4GHAeslxLntR69wcO0_ME-4M11NDpZrydcfM6Ly9hnnNx28clZPMSE7_Q4p1icuXfK7iqCRdLB4TnmYmKwfif6MO5soWZ-jp4MesruxeFeod9fPv86_1Zd_Pj6_fzTRWUEb0vVuK4XThvOhO161lrWUj1wLY0UnXWCdLVxjWka0jHd01raviXMWiFN2zPZ8xX6uPedl37jrHGhJD2pOfmNTtcqaq_-VoJfqzFeKVhew2FVK_T2YJDiFjZQ1MZn46YJpotLVlTwGroQnAL65h_0Mi4pwHh3FKWUkBqod3vKpJhzcsOxGUrULlYFsapdrHAA_eph_0f2PkcA3u-BDFIYXXpQ9L9-rw_V1zGMW_hxtBSEcTDt-C2hpbwN</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>Zhang, Yu-lin</creator><creator>Yao, Yun-tai</creator><creator>Fang, Neng-xin</creator><creator>Zhou, Cheng-hui</creator><creator>Gong, Jun-song</creator><creator>Li, Li-huan</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140601</creationdate><title>Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats</title><author>Zhang, Yu-lin ; Yao, Yun-tai ; Fang, Neng-xin ; Zhou, Cheng-hui ; Gong, Jun-song ; Li, Li-huan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c538t-6e9b5eac325d9b28d281af3a7c759de5094ce6c66092ab147db802dd57c8b27b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Anesthetics, Inhalation - therapeutic use</topic><topic>Animals</topic><topic>Autophagy - drug effects</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cardiotonic Agents - therapeutic use</topic><topic>Heart - drug effects</topic><topic>Immunology</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medical Microbiology</topic><topic>Methyl Ethers - therapeutic use</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - etiology</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Reperfusion Injury - complications</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardium - pathology</topic><topic>Original</topic><topic>original-article</topic><topic>Pharmacology/Toxicology</topic><topic>Rats, Sprague-Dawley</topic><topic>SD大鼠</topic><topic>Vaccine</topic><topic>Western印迹</topic><topic>七氟醚</topic><topic>后处理</topic><topic>心肌组织</topic><topic>心脏</topic><topic>自噬基因</topic><topic>通量</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yu-lin</creatorcontrib><creatorcontrib>Yao, Yun-tai</creatorcontrib><creatorcontrib>Fang, Neng-xin</creatorcontrib><creatorcontrib>Zhou, Cheng-hui</creatorcontrib><creatorcontrib>Gong, Jun-song</creatorcontrib><creatorcontrib>Li, Li-huan</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</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>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>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Acta pharmacologica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yu-lin</au><au>Yao, Yun-tai</au><au>Fang, Neng-xin</au><au>Zhou, Cheng-hui</au><au>Gong, Jun-song</au><au>Li, Li-huan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats</atitle><jtitle>Acta pharmacologica Sinica</jtitle><stitle>Acta Pharmacol Sin</stitle><addtitle>Acta Pharmacologica Sinica</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>35</volume><issue>6</issue><spage>758</spage><epage>769</epage><pages>758-769</pages><issn>1671-4083</issn><eissn>1745-7254</eissn><abstract>Aim： Sevoflurane postconditioning （SpostC） has been shown to protect the heart from ischemia-reperfusion （I/R） injury. In this study, we examined whether SpostC affected autophagic flux in myocardial tissues that contributed to its cardioprotective effects in rats following acute I/R injury.
Methods： SD rats underwent 30 min of left anterior descending coronary artery ligation followed by 120 min of reperfusion. The rats were subjected to inhalation of 2.4% （v/v） sevoflurane during the first 5 min of reperfusion, and chloroquine （10 mg/kg, ip） was injected 1 h before I/R. Myocardial infarct size was estimated using TTC staining. Autophagosomes in myocardial tissues were detected under TEM. Expression of LC3B-II, beclin-1, p62/SQSTM1, cathepsin B, caspase-3 and cleaved PARP was assessed using Western blot analysis. Plasma cardiac troponin I was measured using ELISA. Cardiomyocyte apoptosis was evaluated with TUNEL staining.
Results： I/R procedure produced severe myocardium infarct and apoptosis accompanied by markedly increased number of autophagosomes, as well as increased levels of LC3B-II, beclin-1 and p62 in myocardial tissues. SpostC significantly reduced infarct size, attenuated myocardial apoptosis, restored intact autophagic flux and improved the lysosomal function in myocardial tissues. Administration of chloroquine that blocked autophagic flux abrogated the cardioprotective effects of SpostC.
Conclusion： SpostC exerts its cardioprotective effects in rats following I/R injury via restoring autophagic flux in myocardial tissues.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24793309</pmid><doi>10.1038/aps.2014.20</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anesthetics, Inhalation - therapeutic use Animals Autophagy - drug effects Biomedical and Life Sciences Biomedicine Cardiotonic Agents - therapeutic use Heart - drug effects Immunology Internal Medicine Male Medical Microbiology Methyl Ethers - therapeutic use Myocardial Infarction - drug therapy Myocardial Infarction - etiology Myocardial Infarction - pathology Myocardial Reperfusion Injury - complications Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - pathology Myocardium - pathology Original original-article Pharmacology/Toxicology Rats, Sprague-Dawley SD大鼠 Vaccine Western印迹 七氟醚 后处理 心肌组织 心脏 自噬基因 通量 |
| title | Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats |
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