Dexmedetomidine alleviates cardiomyocyte apoptosis and cardiac dysfunction may be associated with inhibition of RhoA/ROCK pathway in mice with myocardial infarction
The global incidence of myocardial infarction has been consistently high, and it is one of the main causes of poor cardiovascular prognosis. Dexmedetomidine (DEX) is a highly selective α2 receptor agonist. Recent studies have found that DEX has a protective effect on myocardial infarction, but its s...
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| description | The global incidence of myocardial infarction has been consistently high, and it is one of the main causes of poor cardiovascular prognosis. Dexmedetomidine (DEX) is a highly selective α2 receptor agonist. Recent studies have found that DEX has a protective effect on myocardial infarction, but its specific mechanism is still unclear. In this experiment, we permanently ligated the anterior descending branch of mice to explore the protective mechanism of DEX against myocardial infarction. Our study found that intraperitoneal injection of DEX for 7 days after myocardial infarction in mice can increase the reduction of ejection fraction (EF) and fractional shortening (FS) caused by myocardial infarction and significantly reduce the release of serum markers. The results of myocardial HE and Sirius red staining suggest that the changes in the myocardial structure of mice after using DEX are reduced. Immunohistochemistry shows that DEX reduces the expression of ROCK1 protein after myocardial infarction. TUNEL staining and the protein expression levels of cleaved caspase-3 and cleaved caspase-9 were used to detect cell apoptosis and results make clear that DEX can reduce the apoptosis caused by myocardial infarction. Western blot experiments showed that DEX can reduce the expression levels of ROCK1 and ROCK2 (Rho-kinase). At the same time, it was observed that DEX improved the Bcl-2/Bax ratio. The above results indicate that DEX reduces cardiomyocyte apoptosis and improves cardiac function likely through inhibiting the RhoA/ROCK signaling pathway. This study may provide new insights into the protective effect of DEX after myocardial infarction in mice.
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| doi_str_mv | 10.1007/s00210-021-02082-6 |
| format | Article |
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Graphical abstract</description><identifier>ISSN: 0028-1298</identifier><identifier>EISSN: 1432-1912</identifier><identifier>DOI: 10.1007/s00210-021-02082-6</identifier><identifier>PMID: 33782744</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adrenergic alpha-2 Receptor Agonists - pharmacology ; Adrenergic alpha-2 Receptor Agonists - therapeutic use ; Animals ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; Bax protein ; Bcl-2 protein ; Biomedical and Life Sciences ; Biomedicine ; Cardiomyocytes ; Caspase-3 ; Caspase-9 ; Dexmedetomidine - pharmacology ; Dexmedetomidine - therapeutic use ; Dose-Response Relationship, Drug ; Heart attacks ; Immunohistochemistry ; Kinases ; Male ; Mice ; Mice, Inbred C57BL ; Myocardial infarction ; Myocardial Infarction - drug therapy ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Neurosciences ; Original Article ; Pharmacology/Toxicology ; Rho-associated kinase ; rho-Associated Kinases - antagonists & inhibitors ; rho-Associated Kinases - metabolism ; rhoA GTP-Binding Protein - antagonists & inhibitors ; rhoA GTP-Binding Protein - metabolism ; RhoA protein ; Signal transduction ; Signal Transduction - drug effects ; Signal Transduction - physiology</subject><ispartof>Naunyn-Schmiedeberg's archives of pharmacology, 2021-07, Vol.394 (7), p.1569-1577</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-3ebb90da2a2180c7a08f92c3c043fb6a8a1b0d41bc5cf21b6b817666122782023</citedby><cites>FETCH-LOGICAL-c375t-3ebb90da2a2180c7a08f92c3c043fb6a8a1b0d41bc5cf21b6b817666122782023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00210-021-02082-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00210-021-02082-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33782744$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Tao</creatorcontrib><creatorcontrib>Gong, Qian</creatorcontrib><creatorcontrib>Wu, Ying</creatorcontrib><creatorcontrib>Shen, Zhiming</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Ge, Shenglin</creatorcontrib><creatorcontrib>Duan, Jing-Si</creatorcontrib><title>Dexmedetomidine alleviates cardiomyocyte apoptosis and cardiac dysfunction may be associated with inhibition of RhoA/ROCK pathway in mice with myocardial infarction</title><title>Naunyn-Schmiedeberg's archives of pharmacology</title><addtitle>Naunyn-Schmiedeberg's Arch Pharmacol</addtitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><description>The global incidence of myocardial infarction has been consistently high, and it is one of the main causes of poor cardiovascular prognosis. Dexmedetomidine (DEX) is a highly selective α2 receptor agonist. Recent studies have found that DEX has a protective effect on myocardial infarction, but its specific mechanism is still unclear. In this experiment, we permanently ligated the anterior descending branch of mice to explore the protective mechanism of DEX against myocardial infarction. Our study found that intraperitoneal injection of DEX for 7 days after myocardial infarction in mice can increase the reduction of ejection fraction (EF) and fractional shortening (FS) caused by myocardial infarction and significantly reduce the release of serum markers. The results of myocardial HE and Sirius red staining suggest that the changes in the myocardial structure of mice after using DEX are reduced. Immunohistochemistry shows that DEX reduces the expression of ROCK1 protein after myocardial infarction. TUNEL staining and the protein expression levels of cleaved caspase-3 and cleaved caspase-9 were used to detect cell apoptosis and results make clear that DEX can reduce the apoptosis caused by myocardial infarction. Western blot experiments showed that DEX can reduce the expression levels of ROCK1 and ROCK2 (Rho-kinase). At the same time, it was observed that DEX improved the Bcl-2/Bax ratio. The above results indicate that DEX reduces cardiomyocyte apoptosis and improves cardiac function likely through inhibiting the RhoA/ROCK signaling pathway. This study may provide new insights into the protective effect of DEX after myocardial infarction in mice.
Graphical abstract</description><subject>Adrenergic alpha-2 Receptor Agonists - pharmacology</subject><subject>Adrenergic alpha-2 Receptor Agonists - therapeutic use</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cardiomyocytes</subject><subject>Caspase-3</subject><subject>Caspase-9</subject><subject>Dexmedetomidine - pharmacology</subject><subject>Dexmedetomidine - therapeutic use</subject><subject>Dose-Response Relationship, Drug</subject><subject>Heart attacks</subject><subject>Immunohistochemistry</subject><subject>Kinases</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Neurosciences</subject><subject>Original Article</subject><subject>Pharmacology/Toxicology</subject><subject>Rho-associated kinase</subject><subject>rho-Associated Kinases - antagonists & inhibitors</subject><subject>rho-Associated Kinases - metabolism</subject><subject>rhoA GTP-Binding Protein - antagonists & inhibitors</subject><subject>rhoA GTP-Binding Protein - metabolism</subject><subject>RhoA protein</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><issn>0028-1298</issn><issn>1432-1912</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc1uGyEUhVHVqHGdvkAXFVLXE19gfpil5fxVtRQpStYIGKYm8gwTwEnmffKgwZ6k2WXBReJ851yJg9BPAqcEoFoEAEogSyMd4DQrv6AZyRnNSE3oVzRLOs8Irfkx-h7CPQCUpCi-oWPGKk6rPJ-hlzPz3JnGRNfZxvYGy-3WPFoZTcBa-sa6bnR6jEkY3BBdsAHLvpk0qXEzhnbX62hdjzs5YpXAEJzeJzT4ycYNtv3GKnsgXItvNm65uLle_cWDjJunZLHJabWZ4P22Q_Q2vbfSH5JP0FErt8H8eLvn6O7i_HZ1la2vL_-slutMs6qIGTNK1dBIKinhoCsJvK2pZhpy1qpSckkUNDlRutAtJapUnFRlWRJK03cAZXP0e8odvHvYmRDFvdv5Pq0UtMjzuuas2lN0orR3IXjTisHbTvpREBD7YsRUjEhDHIoRZTL9eoveqfTf_y3vTSSATUBIUv_P-I_dn8S-ApF_nBk</recordid><startdate>20210701</startdate><enddate>20210701</enddate><creator>Sun, Tao</creator><creator>Gong, Qian</creator><creator>Wu, Ying</creator><creator>Shen, Zhiming</creator><creator>Zhang, Yan</creator><creator>Ge, Shenglin</creator><creator>Duan, Jing-Si</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20210701</creationdate><title>Dexmedetomidine alleviates cardiomyocyte apoptosis and cardiac dysfunction may be associated with inhibition of RhoA/ROCK pathway in mice with myocardial infarction</title><author>Sun, Tao ; Gong, Qian ; Wu, Ying ; Shen, Zhiming ; Zhang, Yan ; Ge, Shenglin ; Duan, Jing-Si</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-3ebb90da2a2180c7a08f92c3c043fb6a8a1b0d41bc5cf21b6b817666122782023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adrenergic alpha-2 Receptor Agonists - pharmacology</topic><topic>Adrenergic alpha-2 Receptor Agonists - therapeutic use</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Bax protein</topic><topic>Bcl-2 protein</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cardiomyocytes</topic><topic>Caspase-3</topic><topic>Caspase-9</topic><topic>Dexmedetomidine - pharmacology</topic><topic>Dexmedetomidine - therapeutic use</topic><topic>Dose-Response Relationship, Drug</topic><topic>Heart attacks</topic><topic>Immunohistochemistry</topic><topic>Kinases</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Neurosciences</topic><topic>Original Article</topic><topic>Pharmacology/Toxicology</topic><topic>Rho-associated kinase</topic><topic>rho-Associated Kinases - antagonists & inhibitors</topic><topic>rho-Associated Kinases - metabolism</topic><topic>rhoA GTP-Binding Protein - antagonists & inhibitors</topic><topic>rhoA GTP-Binding Protein - metabolism</topic><topic>RhoA protein</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Tao</creatorcontrib><creatorcontrib>Gong, Qian</creatorcontrib><creatorcontrib>Wu, Ying</creatorcontrib><creatorcontrib>Shen, Zhiming</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Ge, Shenglin</creatorcontrib><creatorcontrib>Duan, Jing-Si</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</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>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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Tao</au><au>Gong, Qian</au><au>Wu, Ying</au><au>Shen, Zhiming</au><au>Zhang, Yan</au><au>Ge, Shenglin</au><au>Duan, Jing-Si</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dexmedetomidine alleviates cardiomyocyte apoptosis and cardiac dysfunction may be associated with inhibition of RhoA/ROCK pathway in mice with myocardial infarction</atitle><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle><stitle>Naunyn-Schmiedeberg's Arch Pharmacol</stitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><date>2021-07-01</date><risdate>2021</risdate><volume>394</volume><issue>7</issue><spage>1569</spage><epage>1577</epage><pages>1569-1577</pages><issn>0028-1298</issn><eissn>1432-1912</eissn><abstract>The global incidence of myocardial infarction has been consistently high, and it is one of the main causes of poor cardiovascular prognosis. Dexmedetomidine (DEX) is a highly selective α2 receptor agonist. Recent studies have found that DEX has a protective effect on myocardial infarction, but its specific mechanism is still unclear. In this experiment, we permanently ligated the anterior descending branch of mice to explore the protective mechanism of DEX against myocardial infarction. Our study found that intraperitoneal injection of DEX for 7 days after myocardial infarction in mice can increase the reduction of ejection fraction (EF) and fractional shortening (FS) caused by myocardial infarction and significantly reduce the release of serum markers. The results of myocardial HE and Sirius red staining suggest that the changes in the myocardial structure of mice after using DEX are reduced. Immunohistochemistry shows that DEX reduces the expression of ROCK1 protein after myocardial infarction. TUNEL staining and the protein expression levels of cleaved caspase-3 and cleaved caspase-9 were used to detect cell apoptosis and results make clear that DEX can reduce the apoptosis caused by myocardial infarction. Western blot experiments showed that DEX can reduce the expression levels of ROCK1 and ROCK2 (Rho-kinase). At the same time, it was observed that DEX improved the Bcl-2/Bax ratio. The above results indicate that DEX reduces cardiomyocyte apoptosis and improves cardiac function likely through inhibiting the RhoA/ROCK signaling pathway. This study may provide new insights into the protective effect of DEX after myocardial infarction in mice.
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| subjects | Adrenergic alpha-2 Receptor Agonists - pharmacology Adrenergic alpha-2 Receptor Agonists - therapeutic use Animals Apoptosis Apoptosis - drug effects Apoptosis - physiology Bax protein Bcl-2 protein Biomedical and Life Sciences Biomedicine Cardiomyocytes Caspase-3 Caspase-9 Dexmedetomidine - pharmacology Dexmedetomidine - therapeutic use Dose-Response Relationship, Drug Heart attacks Immunohistochemistry Kinases Male Mice Mice, Inbred C57BL Myocardial infarction Myocardial Infarction - drug therapy Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Neurosciences Original Article Pharmacology/Toxicology Rho-associated kinase rho-Associated Kinases - antagonists & inhibitors rho-Associated Kinases - metabolism rhoA GTP-Binding Protein - antagonists & inhibitors rhoA GTP-Binding Protein - metabolism RhoA protein Signal transduction Signal Transduction - drug effects Signal Transduction - physiology |
| title | Dexmedetomidine alleviates cardiomyocyte apoptosis and cardiac dysfunction may be associated with inhibition of RhoA/ROCK pathway in mice with myocardial infarction |
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