| Title | Effect of sulfur dioxide preconditioning on rat myocardial ischemia/reperfusion injury by inducing endoplasmic reticulum stress |
| Authors | Wang, Xin-Bao Huang, Xiao-Mei Ochs, Todd Li, Xue-Ying Jin, Hong-Fang Tang, Chao-Shu Du, Jun-Bao |
| Affiliation | Peking Univ, Dept Pediat, Hosp 1, Beijing 100034, Peoples R China. Univ Illinois, Sch Med, Chicago, IL USA. Peking Univ, Dept Stat, Hosp 1, Beijing 100034, Peoples R China. Minist Educ, Key Lab Mol Cardiol, Beijing 100191, Peoples R China. Peking Univ, Dept Physiol & Pathophysiol, Hlth Sci Ctr, Beijing 100191, Peoples R China. |
| Keywords | Sulfur dioxide Preconditioning Ischemia reperfusion Endoplasmic reticulum stress ISCHEMIA-REPERFUSION INJURY SERUM SULFITE EARLY REVASCULARIZATION TRANSITION PORE NITRIC-OXIDE CELL-DEATH PROTECTS DERIVATIVES INHIBITION EXPRESSION |
| Issue Date | 2011 |
| Publisher | basic research in cardiology |
| Citation | BASIC RESEARCH IN CARDIOLOGY.2011,106,(5),865-878. |
| Abstract | Sulfur dioxide has recently been found to be produced endogenously in the cardiovascular system and have important positive biological effects. However, it is unknown whether sulfur dioxide preconditioning has a protective effect on rat myocardial ischemia/reperfusion (I/R) injury and whether this process involves endoplasmic reticulum stress (ERS). In this study, we showed that preconditioning with sulfur dioxide 10 min before ischemia (with a low concentration of sulfur dioxide of 1-10 mu mol/kg) could reduce myocardial infarct size and plasma activities of lactate dehydrogenase and creatine kinase in rats with I/R in vivo. Sulfur dioxide preconditioning also reduced myocardium apoptosis induced by I/R. In addition, sulfur dioxide preconditioning increased cardiac function in vitro. Sulfur dioxide preconditioning induced expression of myocardial glucose-regulated protein 78 (GRP78) and phosphorylated eukaryotic initiation of the factor 2 alpha-subunit (p-eIF2 alpha) prior to myocardial I/R but suppressed expression of myocardial GRP78, C/EBP homologous protein, and p-eIF2 alpha during myocardial I/R, in association with improved myocardial injury in vivo and in vitro. Pretreatment with dithiothreitol, an ERS stimulator mimicked the above cardioprotective effect. However, pretreatment with the ERS inhibitor 4-phenylbutyrate reversed the cardioprotection provided by sulfur dioxide preconditioning. These data indicated that sulfur dioxide preconditioning reduced I/R-induced myocardial injury in vivo and in vitro, and that augmenting ERS by sulfur dioxide preconditioning prior to I/R contributed to protection against myocardial I/R injury. |
| URI | http://hdl.handle.net/20.500.11897/160199 |
| ISSN | 0300-8428 |
| DOI | 10.1007/s00395-011-0176-x |
| Indexed | SCI(E) PubMed |
| Appears in Collections: | 第一医院 |
