title: Protective effect of erythropoietin against myocardial injury in rats with sepsis and its underlying mechanisms.
abstract: The aim of this study was to investigate the protective effect of erythropoietin (EPO) against acute myocardial injury and its underlying mechanisms. Mice (n=146) were randomly divided in a double‑blind manner into four groups, sham, Rocephin, EPO and sepsis, and mortality was observed on the seventh day after cecal ligation and puncture. In addition, a total of 252 rats were randomly divided into three groups, sham, EPO and sepsis, and indicators of cardiac function, inflammatory mediators and serum creatine kinase levels were assessed. Mitochondrial membrane potential, cell apoptosis and nuclear factor κ‑light‑chain‑enhancer of activated B cells (NF‑κB) p65 expression levels were detected using flow cytometry. Following intervention with EPO, the mortality rate in mice with sepsis was significantly reduced and the cardiac function of septic rats was significantly improved. In addition, the levels of inflammatory mediators, serum creatine kinase and apoptosis and the myocardial mitochondrial membrane potential and expression of NF‑κB p65 in cardiac tissue were all improved following EPO treatment, and the differences between the results for the sepsis and EPO groups were statistically significant (P<0.05). These findings suggest that EPO reduces the myocardial inflammatory response in septic rats, attenuates the reduction in mitochondrial membrane potential and inhibits myocardial cell apoptosis by reducing NF‑κB p65 expression, and therefore exerts a protective effect in the myocardium.
authors.affiliation: Department of Emergency, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China.
authors.forename: Xinliang
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Critical Care Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China.
authors.forename: Shimin
authors.initials: S
authors.lastname: Dong
authors.affiliation: Department of Emergency, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China.
authors.forename: Yanjun
authors.initials: Y
authors.lastname: Qin
authors.affiliation: Department of Emergency, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China.
authors.forename: Xiaohua
authors.initials: X
authors.lastname: Bian
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015415:Biomarkers; D009202:Cardiomyopathies / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology; D002316:Cardiotonic Agents / Q000494:pharmacology*; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004921:Erythropoietin / Q000494:pharmacology*; D006439:Hemodynamics; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D051379:Mice; D009026:Mortality; D051381:Rats; D018805:Sepsis / Q000150:complications*; D013997:Time Factors; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D015415:Biomarkers; D002316:Cardiotonic Agents; D016207:Cytokines; D018836:Inflammation Mediators; D051996:Transcription Factor RelA; D004921:Erythropoietin