title: Dimethyl sulfoxide attenuates hydrogen peroxide-induced injury in cardiomyocytes via heme oxygenase-1.
abstract: The antioxidant property of dimethyl sulfoxide (DMSO) was formerly attributed to its direct effects. Our former study showed that DMSO is able to induce heme oxygenase-1 (HO-1) expression in endothelial cells, which is a potent antioxidant enzyme. In this study, we hypothesized that the antioxidant effects of DMSO in cardiomyocytes are mediated or partially mediated by increased HO-1 expression. Therefore, we investigated whether DMSO exerts protective effects against H2 O2 -induced oxidative damage in cardiomyocytes, and whether HO-1 is involved in DMSO-imparted protective effects, and we also explore the underlying mechanism of DMSO-induced HO-1 expression. Our study demonstrated that DMSO pretreatment showed a cytoprotective effect against H2 O2 -induced oxidative damage (impaired cell viability, increased apopototic cells rate and caspase-3 level, and increased release of LDH and CK) and this process is partially mediated by HO-1 upregulation. Furthermore, our data showed that the activation of p38 MAPK and Nrf2 translocation are involved in the HO-1 upregulation induced by DMSO. This study reports for the first time that the cytoprotective effect of DMSO in cardiomyocytes is partially mediated by HO-1, which may further explain the mechanisms by which DMSO exerts cardioprotection on H2 O2 injury. J. Cell. Biochem. 115: 1159-1165, 2014. © 2013 Wiley Periodicals, Inc.
authors.affiliation: Department of Gynecology and Obstetrics, Shanghai Minhang District Central Hospital, Shanghai, China.
authors.forename: Wang
authors.initials: W
authors.lastname: Man
authors.forename: Ding
authors.initials: D
authors.lastname: Ming
authors.forename: Du
authors.initials: D
authors.lastname: Fang
authors.forename: Liang
authors.initials: L
authors.lastname: Chao
authors.forename: Cang
authors.initials: C
authors.lastname: Jing
mesh_terms: D021581:Active Transport, Cell Nucleus / Q000187:drug effects; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D053148:Caspase 3 / Q000378:metabolism; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D003451:Cryoprotective Agents / Q000494:pharmacology; D004121:Dimethyl Sulfoxide / Q000494:pharmacology*; D051547:Heme Oxygenase-1 / Q000378:metabolism*; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000378:metabolism; D016877:Oxidants / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D015854:Up-Regulation / Q000187:drug effects; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D003451:Cryoprotective Agents; D051267:NF-E2-Related Factor 2; C495637:Nfe2l2 protein, rat; D016877:Oxidants; D006861:Hydrogen Peroxide; D051547:Heme Oxygenase-1; D048051:p38 Mitogen-Activated Protein Kinases; D053148:Caspase 3; D004121:Dimethyl Sulfoxide
keywords: CARDIOMYOCYTES; DIMETHYL SULFOXIDE; HEME OXYGENASE-1; HYDROGEN PEROXIDE