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
Hauptverfasser: Yin, Wenchao, Wang, Chunyan, Peng, Yue, Yuan, Wenlin, Zhang, Zhongjun, Liu, Hong, Xia, Zhengyuan, Ren, Congcai, Qian, Jinqiao
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Sprache:eng
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Zusammenfassung: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  
ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-020-05456-w