Dexmedetomidine alleviates H2O2-induced oxidative stress and cell necroptosis through activating of α2-adrenoceptor in H9C2 cells
Oxidative stress induced necroptosis is important in myocardial ischemia/reperfusion injury. Dexmedetomidine (Dex), an α2-adrenoceptor (α2-AR) agonist, has protective effect on oxidative stress induced cell apoptosis, but effects of Dex and Dex-mediated α2-AR activation on oxidant induced necroptosi...
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| Veröffentlicht in: | Molecular biology reports 2020-05, Vol.47 (5), p.3629-3639 |
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| creator | Yin, Wenchao Wang, Chunyan Peng, Yue Yuan, Wenlin Zhang, Zhongjun Liu, Hong Xia, Zhengyuan Ren, Congcai Qian, Jinqiao |
| description | Oxidative stress induced necroptosis is important in myocardial ischemia/reperfusion injury. Dexmedetomidine (Dex), an α2-adrenoceptor (α2-AR) agonist, has protective effect on oxidative stress induced cell apoptosis, but effects of Dex and Dex-mediated α2-AR activation on oxidant induced necroptosis was unclear. H9C2 cardiomyocytes were pre-treated with or without Dex and α2-AR antagonist yohimbine hydrochloride (YOH) before being exposed to H
2
O
2
to induce oxidative cellular damage. Cell viability and lactate dehydrogenase (LDH) were detected by ELISA kits, protein expressions of Heme Oxygenase 1(HO-1), receptor interacting protein kinase 1 (RIPK1) and receptor interacting protein kinase 3 (RIPK3) were observed by WB, and TUNEL was used to detected cell apoptosis. H
2
O
2
significantly decreased cell viability and increased LDH release and necroptotic and apoptotic cell deaths (all
p
|
| doi_str_mv | 10.1007/s11033-020-05456-w |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2577745885</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2577745885</sourcerecordid><originalsourceid>FETCH-LOGICAL-c311w-9ff16dc6c39e0792590b122c04c1882d0fbe708b8d70067911639b5ed5a5530e3</originalsourceid><addsrcrecordid>eNp9kMFOGzEQQK2qSKTAD3CyxNnt2F6vd48obUklJC7lbDn2bHC0sVN7Q-DaP-JH-Ka6CRI3TnN5b0bzCLnk8JUD6G-Fc5CSgQAGqlEt238iM660ZE2vu89kBhI4azrFT8mXUtYA0HCtZuTvd3zaoMcpbYIPEakdR3wMdsJCF-JOsBD9zqGn6Sl4O4VHpGXKWAq10VOH40gjupy2Uyqh0Okhp93qgVpX0YrHFU0DfX0RzPqMMTmsYKYh0kU_Fwe_nJOTwY4FL97mGbn_-eP3fMFu725-za9vmZOc71k_DLz1rnWyR9C9UD0suRAOGse7TngYlqihW3ZeA7S657yV_VKhV1YpCSjPyNVx7zanPzssk1mnXY71pBFKa92orlOVEkeqPlVKxsFsc9jY_Gw4mP-tzbG1qa3NobXZV0kepVLhuML8vvoD6x_FkYPc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2577745885</pqid></control><display><type>article</type><title>Dexmedetomidine alleviates H2O2-induced oxidative stress and cell necroptosis through activating of α2-adrenoceptor in H9C2 cells</title><source>Springer Nature - Complete Springer Journals</source><creator>Yin, Wenchao ; Wang, Chunyan ; Peng, Yue ; Yuan, Wenlin ; Zhang, Zhongjun ; Liu, Hong ; Xia, Zhengyuan ; Ren, Congcai ; Qian, Jinqiao</creator><creatorcontrib>Yin, Wenchao ; Wang, Chunyan ; Peng, Yue ; Yuan, Wenlin ; Zhang, Zhongjun ; Liu, Hong ; Xia, Zhengyuan ; Ren, Congcai ; Qian, Jinqiao</creatorcontrib><description>Oxidative stress induced necroptosis is important in myocardial ischemia/reperfusion injury. Dexmedetomidine (Dex), an α2-adrenoceptor (α2-AR) agonist, has protective effect on oxidative stress induced cell apoptosis, but effects of Dex and Dex-mediated α2-AR activation on oxidant induced necroptosis was unclear. H9C2 cardiomyocytes were pre-treated with or without Dex and α2-AR antagonist yohimbine hydrochloride (YOH) before being exposed to H
2
O
2
to induce oxidative cellular damage. Cell viability and lactate dehydrogenase (LDH) were detected by ELISA kits, protein expressions of Heme Oxygenase 1(HO-1), receptor interacting protein kinase 1 (RIPK1) and receptor interacting protein kinase 3 (RIPK3) were observed by WB, and TUNEL was used to detected cell apoptosis. H
2
O
2
significantly decreased cell viability and increased LDH release and necroptotic and apoptotic cell deaths (all
p
< 0.05, H
2
O
2
vs. Control). Dex preconditioning alleviated these injuries induced by H
2
O
2
. Dex preconditioning significantly increased expression of protein HO-1 and decreased expressions of proteins RIPK1 and RIPK3 induced by H
2
O
2
, while all these protective effects of Dex were reversed by YOH (all
p
< 0.05, Dex + H
2
O
2
vs. H
2
O
2
; and YOH + Dex + H
2
O
2
vs. Dex + H
2
O
2
). However, YOH did not prevent this protective effect of Dex against H
2
O
2
induced apoptosis (YOH + Dex + H
2
O
2
vs. Dex + H
2
O
2
,
p
> 0.05). These findings indicated that Dex attenuates H
2
O
2
induced cardiomyocyte necroptotic and apoptotic cell death respectively dependently and independently of α2-AR activation.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-020-05456-w</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Adrenergic receptors ; Animal Anatomy ; Animal Biochemistry ; Apoptosis ; Biomedical and Life Sciences ; Cardiomyocytes ; Cell death ; Cell viability ; Heme ; Histology ; Hydrogen peroxide ; Ischemia ; Kinases ; L-Lactate dehydrogenase ; Lactic acid ; Life Sciences ; Morphology ; Myocardial ischemia ; Necroptosis ; Original Article ; Oxidants ; Oxidative stress ; Oxygenase ; Protein kinase ; Proteins ; Reperfusion ; Yohimbine</subject><ispartof>Molecular biology reports, 2020-05, Vol.47 (5), p.3629-3639</ispartof><rights>Springer Nature B.V. 2020</rights><rights>Springer Nature B.V. 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c311w-9ff16dc6c39e0792590b122c04c1882d0fbe708b8d70067911639b5ed5a5530e3</citedby><cites>FETCH-LOGICAL-c311w-9ff16dc6c39e0792590b122c04c1882d0fbe708b8d70067911639b5ed5a5530e3</cites><orcidid>0000-0003-1441-5971</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-020-05456-w$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-020-05456-w$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids></links><search><creatorcontrib>Yin, Wenchao</creatorcontrib><creatorcontrib>Wang, Chunyan</creatorcontrib><creatorcontrib>Peng, Yue</creatorcontrib><creatorcontrib>Yuan, Wenlin</creatorcontrib><creatorcontrib>Zhang, Zhongjun</creatorcontrib><creatorcontrib>Liu, Hong</creatorcontrib><creatorcontrib>Xia, Zhengyuan</creatorcontrib><creatorcontrib>Ren, Congcai</creatorcontrib><creatorcontrib>Qian, Jinqiao</creatorcontrib><title>Dexmedetomidine alleviates H2O2-induced oxidative stress and cell necroptosis through activating of α2-adrenoceptor in H9C2 cells</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><description>Oxidative stress induced necroptosis is important in myocardial ischemia/reperfusion injury. Dexmedetomidine (Dex), an α2-adrenoceptor (α2-AR) agonist, has protective effect on oxidative stress induced cell apoptosis, but effects of Dex and Dex-mediated α2-AR activation on oxidant induced necroptosis was unclear. H9C2 cardiomyocytes were pre-treated with or without Dex and α2-AR antagonist yohimbine hydrochloride (YOH) before being exposed to H
2
O
2
to induce oxidative cellular damage. Cell viability and lactate dehydrogenase (LDH) were detected by ELISA kits, protein expressions of Heme Oxygenase 1(HO-1), receptor interacting protein kinase 1 (RIPK1) and receptor interacting protein kinase 3 (RIPK3) were observed by WB, and TUNEL was used to detected cell apoptosis. H
2
O
2
significantly decreased cell viability and increased LDH release and necroptotic and apoptotic cell deaths (all
p
< 0.05, H
2
O
2
vs. Control). Dex preconditioning alleviated these injuries induced by H
2
O
2
. Dex preconditioning significantly increased expression of protein HO-1 and decreased expressions of proteins RIPK1 and RIPK3 induced by H
2
O
2
, while all these protective effects of Dex were reversed by YOH (all
p
< 0.05, Dex + H
2
O
2
vs. H
2
O
2
; and YOH + Dex + H
2
O
2
vs. Dex + H
2
O
2
). However, YOH did not prevent this protective effect of Dex against H
2
O
2
induced apoptosis (YOH + Dex + H
2
O
2
vs. Dex + H
2
O
2
,
p
> 0.05). These findings indicated that Dex attenuates H
2
O
2
induced cardiomyocyte necroptotic and apoptotic cell death respectively dependently and independently of α2-AR activation.</description><subject>Adrenergic receptors</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiomyocytes</subject><subject>Cell death</subject><subject>Cell viability</subject><subject>Heme</subject><subject>Histology</subject><subject>Hydrogen peroxide</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>L-Lactate dehydrogenase</subject><subject>Lactic acid</subject><subject>Life Sciences</subject><subject>Morphology</subject><subject>Myocardial ischemia</subject><subject>Necroptosis</subject><subject>Original Article</subject><subject>Oxidants</subject><subject>Oxidative stress</subject><subject>Oxygenase</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Reperfusion</subject><subject>Yohimbine</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kMFOGzEQQK2qSKTAD3CyxNnt2F6vd48obUklJC7lbDn2bHC0sVN7Q-DaP-JH-Ka6CRI3TnN5b0bzCLnk8JUD6G-Fc5CSgQAGqlEt238iM660ZE2vu89kBhI4azrFT8mXUtYA0HCtZuTvd3zaoMcpbYIPEakdR3wMdsJCF-JOsBD9zqGn6Sl4O4VHpGXKWAq10VOH40gjupy2Uyqh0Okhp93qgVpX0YrHFU0DfX0RzPqMMTmsYKYh0kU_Fwe_nJOTwY4FL97mGbn_-eP3fMFu725-za9vmZOc71k_DLz1rnWyR9C9UD0suRAOGse7TngYlqihW3ZeA7S657yV_VKhV1YpCSjPyNVx7zanPzssk1mnXY71pBFKa92orlOVEkeqPlVKxsFsc9jY_Gw4mP-tzbG1qa3NobXZV0kepVLhuML8vvoD6x_FkYPc</recordid><startdate>20200501</startdate><enddate>20200501</enddate><creator>Yin, Wenchao</creator><creator>Wang, Chunyan</creator><creator>Peng, Yue</creator><creator>Yuan, Wenlin</creator><creator>Zhang, Zhongjun</creator><creator>Liu, Hong</creator><creator>Xia, Zhengyuan</creator><creator>Ren, Congcai</creator><creator>Qian, Jinqiao</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><orcidid>https://orcid.org/0000-0003-1441-5971</orcidid></search><sort><creationdate>20200501</creationdate><title>Dexmedetomidine alleviates H2O2-induced oxidative stress and cell necroptosis through activating of α2-adrenoceptor in H9C2 cells</title><author>Yin, Wenchao ; Wang, Chunyan ; Peng, Yue ; Yuan, Wenlin ; Zhang, Zhongjun ; Liu, Hong ; Xia, Zhengyuan ; Ren, Congcai ; Qian, Jinqiao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c311w-9ff16dc6c39e0792590b122c04c1882d0fbe708b8d70067911639b5ed5a5530e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adrenergic receptors</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiomyocytes</topic><topic>Cell death</topic><topic>Cell viability</topic><topic>Heme</topic><topic>Histology</topic><topic>Hydrogen peroxide</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>L-Lactate dehydrogenase</topic><topic>Lactic acid</topic><topic>Life Sciences</topic><topic>Morphology</topic><topic>Myocardial ischemia</topic><topic>Necroptosis</topic><topic>Original Article</topic><topic>Oxidants</topic><topic>Oxidative stress</topic><topic>Oxygenase</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Reperfusion</topic><topic>Yohimbine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yin, Wenchao</creatorcontrib><creatorcontrib>Wang, Chunyan</creatorcontrib><creatorcontrib>Peng, Yue</creatorcontrib><creatorcontrib>Yuan, Wenlin</creatorcontrib><creatorcontrib>Zhang, Zhongjun</creatorcontrib><creatorcontrib>Liu, Hong</creatorcontrib><creatorcontrib>Xia, Zhengyuan</creatorcontrib><creatorcontrib>Ren, Congcai</creatorcontrib><creatorcontrib>Qian, Jinqiao</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>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>Science Database</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 Basic</collection><collection>Genetics Abstracts</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yin, Wenchao</au><au>Wang, Chunyan</au><au>Peng, Yue</au><au>Yuan, Wenlin</au><au>Zhang, Zhongjun</au><au>Liu, Hong</au><au>Xia, Zhengyuan</au><au>Ren, Congcai</au><au>Qian, Jinqiao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dexmedetomidine alleviates H2O2-induced oxidative stress and cell necroptosis through activating of α2-adrenoceptor in H9C2 cells</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><date>2020-05-01</date><risdate>2020</risdate><volume>47</volume><issue>5</issue><spage>3629</spage><epage>3639</epage><pages>3629-3639</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Oxidative stress induced necroptosis is important in myocardial ischemia/reperfusion injury. Dexmedetomidine (Dex), an α2-adrenoceptor (α2-AR) agonist, has protective effect on oxidative stress induced cell apoptosis, but effects of Dex and Dex-mediated α2-AR activation on oxidant induced necroptosis was unclear. H9C2 cardiomyocytes were pre-treated with or without Dex and α2-AR antagonist yohimbine hydrochloride (YOH) before being exposed to H
2
O
2
to induce oxidative cellular damage. Cell viability and lactate dehydrogenase (LDH) were detected by ELISA kits, protein expressions of Heme Oxygenase 1(HO-1), receptor interacting protein kinase 1 (RIPK1) and receptor interacting protein kinase 3 (RIPK3) were observed by WB, and TUNEL was used to detected cell apoptosis. H
2
O
2
significantly decreased cell viability and increased LDH release and necroptotic and apoptotic cell deaths (all
p
< 0.05, H
2
O
2
vs. Control). Dex preconditioning alleviated these injuries induced by H
2
O
2
. Dex preconditioning significantly increased expression of protein HO-1 and decreased expressions of proteins RIPK1 and RIPK3 induced by H
2
O
2
, while all these protective effects of Dex were reversed by YOH (all
p
< 0.05, Dex + H
2
O
2
vs. H
2
O
2
; and YOH + Dex + H
2
O
2
vs. Dex + H
2
O
2
). However, YOH did not prevent this protective effect of Dex against H
2
O
2
induced apoptosis (YOH + Dex + H
2
O
2
vs. Dex + H
2
O
2
,
p
> 0.05). These findings indicated that Dex attenuates H
2
O
2
induced cardiomyocyte necroptotic and apoptotic cell death respectively dependently and independently of α2-AR activation.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><doi>10.1007/s11033-020-05456-w</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-1441-5971</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Molecular biology reports, 2020-05, Vol.47 (5), p.3629-3639 |
| issn | 0301-4851 1573-4978 |
| language | eng |
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| source | Springer Nature - Complete Springer Journals |
| subjects | Adrenergic receptors Animal Anatomy Animal Biochemistry Apoptosis Biomedical and Life Sciences Cardiomyocytes Cell death Cell viability Heme Histology Hydrogen peroxide Ischemia Kinases L-Lactate dehydrogenase Lactic acid Life Sciences Morphology Myocardial ischemia Necroptosis Original Article Oxidants Oxidative stress Oxygenase Protein kinase Proteins Reperfusion Yohimbine |
| title | Dexmedetomidine alleviates H2O2-induced oxidative stress and cell necroptosis through activating of α2-adrenoceptor in H9C2 cells |
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