机构：[1]Department of Anesthesiology, First Afliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China[2]Department of Anesthesiology, Sichuan Provincial Orthopedic Hospital, Chengdu 610041, Sichuan, China[3]Department of Anesthesiology, Shenzhen People’s Hospital and Shenzhen Anesthesiology Engineering Center, The Second Clinical Medical College of Jinan University,深圳市康宁医院深圳市人民医院深圳医学信息中心[4]Department of Anesthesiology, The Eighth Afliated Hospital of Sun Yat-Sen University, Shenzhen 518034, China深圳市康宁医院深圳医学信息中心中国医学科学院阜外医院深圳医院[5]Department of Anaesthesiology and Pain Medicine,University of California Davis Health System, Sacramento,CA, USA
Oxidative stress induced necroptosis is important in myocardial ischemia/reperfusion injury. Dexmedetomidine (Dex), an alpha 2-adrenoceptor (alpha 2-AR) agonist, has protective effect on oxidative stress induced cell apoptosis, but effects of Dex and Dex-mediated alpha 2-AR activation on oxidant induced necroptosis was unclear. H9C2 cardiomyocytes were pre-treated with or without Dex and alpha 2-AR antagonist yohimbine hydrochloride (YOH) before being exposed to H2O2 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. H2O2 significantly decreased cell viability and increased LDH release and necroptotic and apoptotic cell deaths (all p < 0.05, H2O2 vs. Control). Dex preconditioning alleviated these injuries induced by H2O2. Dex preconditioning significantly increased expression of protein HO-1 and decreased expressions of proteins RIPK1 and RIPK3 induced by H2O2, while all these protective effects of Dex were reversed by YOH (all p < 0.05, Dex + H2O2 vs. H2O2; and YOH + Dex + H2O2 vs. Dex + H2O2). However, YOH did not prevent this protective effect of Dex against H2O2 induced apoptosis (YOH + Dex + H2O2 vs. Dex + H2O2, p > 0.05). These findings indicated that Dex attenuates H2O2 induced cardiomyocyte necroptotic and apoptotic cell death respectively dependently and independently of alpha 2-AR activation.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81801947]; Shenzhen Science and Technology Innovation Committee [JCYJ20180305180809671]
第一作者机构：[1]Department of Anesthesiology, First Afliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China[2]Department of Anesthesiology, Sichuan Provincial Orthopedic Hospital, Chengdu 610041, Sichuan, China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Yin Wenchao,Wang Chunyan,Peng Yue,et al.Dexmedetomidine alleviates H2O2-induced oxidative stress and cell necroptosis through activating of alpha 2-adrenoceptor in H9C2 cells[J].MOLECULAR BIOLOGY REPORTS.2020,47(5):3629-3639.doi:10.1007/s11033-020-05456-w.
APA：
Yin, Wenchao,Wang, Chunyan,Peng, Yue,Yuan, Wenlin,Zhang, Zhongjun...&Qian, Jinqiao.(2020).Dexmedetomidine alleviates H2O2-induced oxidative stress and cell necroptosis through activating of alpha 2-adrenoceptor in H9C2 cells.MOLECULAR BIOLOGY REPORTS,47,(5)
MLA：
Yin, Wenchao,et al."Dexmedetomidine alleviates H2O2-induced oxidative stress and cell necroptosis through activating of alpha 2-adrenoceptor in H9C2 cells".MOLECULAR BIOLOGY REPORTS 47..5(2020):3629-3639
