Dexmedetomidine alleviates H 2 O 2 -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 |
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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
O
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
O
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 |
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O
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
O
significantly decreased cell viability and increased LDH release and necroptotic and apoptotic cell deaths (all p < 0.05, H
O
vs. Control). Dex preconditioning alleviated these injuries induced by H
O
. Dex preconditioning significantly increased expression of protein HO-1 and decreased expressions of proteins RIPK1 and RIPK3 induced by H
O
, while all these protective effects of Dex were reversed by YOH (all p < 0.05, Dex + H
O
vs. H
O
; and YOH + Dex + H
O
vs. Dex + H
O
). However, YOH did not prevent this protective effect of Dex against H
O
induced apoptosis (YOH + Dex + H
O
vs. Dex + H
O
, p > 0.05). These findings indicated that Dex attenuates H
O
induced cardiomyocyte necroptotic and apoptotic cell death respectively dependently and independently of α2-AR activation.</description><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-020-05456-w</identifier><identifier>PMID: 32342432</identifier><language>eng</language><publisher>Netherlands</publisher><subject>Animals ; Apoptosis - drug effects ; Cell Culture Techniques ; Cell Death - drug effects ; Cell Line ; Cell Survival - drug effects ; Dexmedetomidine - metabolism ; Dexmedetomidine - pharmacology ; Heme Oxygenase-1 - metabolism ; Hydrogen Peroxide - pharmacology ; Myocardial Reperfusion Injury - metabolism ; Myocytes, Cardiac - metabolism ; Necroptosis - drug effects ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Rats ; Receptors, Adrenergic - metabolism ; Receptors, Adrenergic, alpha-2 - drug effects ; Receptors, Adrenergic, alpha-2 - metabolism ; Signal Transduction - drug effects</subject><ispartof>Molecular biology reports, 2020-05, Vol.47 (5), p.3629</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0003-1441-5971</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32342432$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></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 H 2 O 2 -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
O
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
O
significantly decreased cell viability and increased LDH release and necroptotic and apoptotic cell deaths (all p < 0.05, H
O
vs. Control). Dex preconditioning alleviated these injuries induced by H
O
. Dex preconditioning significantly increased expression of protein HO-1 and decreased expressions of proteins RIPK1 and RIPK3 induced by H
O
, while all these protective effects of Dex were reversed by YOH (all p < 0.05, Dex + H
O
vs. H
O
; and YOH + Dex + H
O
vs. Dex + H
O
). However, YOH did not prevent this protective effect of Dex against H
O
induced apoptosis (YOH + Dex + H
O
vs. Dex + H
O
, p > 0.05). These findings indicated that Dex attenuates H
O
induced cardiomyocyte necroptotic and apoptotic cell death respectively dependently and independently of α2-AR activation.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Cell Culture Techniques</subject><subject>Cell Death - drug effects</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Dexmedetomidine - metabolism</subject><subject>Dexmedetomidine - pharmacology</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Necroptosis - drug effects</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Receptors, Adrenergic - metabolism</subject><subject>Receptors, Adrenergic, alpha-2 - drug effects</subject><subject>Receptors, Adrenergic, alpha-2 - metabolism</subject><subject>Signal Transduction - drug effects</subject><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFzjtOAzEUBVALCZHw2QAFehsw-DcMqQNoOhr6yNgvidGMPfLz5LMB9sNGWBMWgpri6jbnSpexaylupRDtHUkptOZCCS4a09zz_Qmby6bV3Czahxk7J3oXQhjZNmdsppU2ymg1Zx-PeBjQY0lD8CEi2L7HXbAFCTpQ8FLDQ_STQw_pELwtYYdAJSMR2OjBYd9DRJfTWBIFgrLNadpswbpKK48bSGv4-lTc-owxOawwQ4jQLZbqZ0-X7HRte8Kr375gN89Pr8uOj9NbvbcacxhsPq7-jut_wTes-FWL</recordid><startdate>202005</startdate><enddate>202005</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><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><orcidid>https://orcid.org/0000-0003-1441-5971</orcidid></search><sort><creationdate>202005</creationdate><title>Dexmedetomidine alleviates H 2 O 2 -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-pubmed_primary_323424323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Cell Culture Techniques</topic><topic>Cell Death - drug effects</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Dexmedetomidine - metabolism</topic><topic>Dexmedetomidine - pharmacology</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Necroptosis - drug effects</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Receptors, Adrenergic - metabolism</topic><topic>Receptors, Adrenergic, alpha-2 - drug effects</topic><topic>Receptors, Adrenergic, alpha-2 - metabolism</topic><topic>Signal Transduction - drug effects</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>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</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 H 2 O 2 -induced oxidative stress and cell necroptosis through activating of α2-adrenoceptor in H9C2 cells</atitle><jtitle>Molecular biology reports</jtitle><addtitle>Mol Biol Rep</addtitle><date>2020-05</date><risdate>2020</risdate><volume>47</volume><issue>5</issue><spage>3629</spage><pages>3629-</pages><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
O
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
O
significantly decreased cell viability and increased LDH release and necroptotic and apoptotic cell deaths (all p < 0.05, H
O
vs. Control). Dex preconditioning alleviated these injuries induced by H
O
. Dex preconditioning significantly increased expression of protein HO-1 and decreased expressions of proteins RIPK1 and RIPK3 induced by H
O
, while all these protective effects of Dex were reversed by YOH (all p < 0.05, Dex + H
O
vs. H
O
; and YOH + Dex + H
O
vs. Dex + H
O
). However, YOH did not prevent this protective effect of Dex against H
O
induced apoptosis (YOH + Dex + H
O
vs. Dex + H
O
, p > 0.05). These findings indicated that Dex attenuates H
O
induced cardiomyocyte necroptotic and apoptotic cell death respectively dependently and independently of α2-AR activation.</abstract><cop>Netherlands</cop><pmid>32342432</pmid><doi>10.1007/s11033-020-05456-w</doi><orcidid>https://orcid.org/0000-0003-1441-5971</orcidid></addata></record> |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Apoptosis - drug effects Cell Culture Techniques Cell Death - drug effects Cell Line Cell Survival - drug effects Dexmedetomidine - metabolism Dexmedetomidine - pharmacology Heme Oxygenase-1 - metabolism Hydrogen Peroxide - pharmacology Myocardial Reperfusion Injury - metabolism Myocytes, Cardiac - metabolism Necroptosis - drug effects Oxidative Stress - drug effects Oxidative Stress - physiology Rats Receptors, Adrenergic - metabolism Receptors, Adrenergic, alpha-2 - drug effects Receptors, Adrenergic, alpha-2 - metabolism Signal Transduction - drug effects |
| title | Dexmedetomidine alleviates H 2 O 2 -induced oxidative stress and cell necroptosis through activating of α2-adrenoceptor in H9C2 cells |
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