title: Etanercept attenuates myocardial ischemia/reperfusion injury by decreasing inflammation and oxidative stress.
abstract: The protective role of etanercept in myocardial ischemia/reperfusion is not well understood. The aim of this study was to investigate whether etanercept modulates neutrophil accumulation, TNF-α induction and oxidative stress in an ischemia/reperfusion injured rat heart model. Rats were randomly exposed to sham operation, myocardial ischemia/reperfusion (MI/R) alone, MI/R+ etanercept. The results demonstrated that compared to MI/R, etanercept reduced myocardial infarction area, myocardial myeloperoxidase (MPO) levels, serum creatinine kinase (CK) and lactate dehydrogenase (LDH) levels, and both serum and myocardial TNF-α production. Etanercept also markedly enhanced the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and reduced the level of malondialdehyde (MDA) in MI/R rats. In summary, our data suggested that etanercept has protective effects against MI/R injury in rats, which may be attributed to attenuating inflammation and oxidative stress.
authors.affiliation: Department of Critical Care Medicine, the Third Hospital of Jinan, Jinan, People's Republic of China.
authors.forename: Mei
authors.initials: M
authors.lastname: Yang
authors.affiliation: Department of Emergency, Shandong Provincial Hospital, Jinan, People's Republic of China.
authors.forename: Jianchang
authors.initials: J
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Qilu Hospital of Shandong University, Jinan, People's Republic of China.
authors.forename: Jing
authors.initials: J
authors.lastname: Zhao
authors.affiliation: Department of Critical Care Medicine, Shandong Provincial Hospital, Jinan, People's Republic of China.
authors.forename: Mei
authors.initials: M
authors.lastname: Meng
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D052279:Creatine Kinase, MB Form / Q000097:blood / Q000378:metabolism; D004195:Disease Models, Animal; D000068800:Etanercept; D005786:Gene Expression Regulation / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000378:metabolism; D007074:Immunoglobulin G / Q000008:administration & dosage / Q000494:pharmacology*; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism*; D045022:Lactate Dehydrogenases / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009203:Myocardial Infarction / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D020556:Neutrophil Infiltration / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D018124:Receptors, Tumor Necrosis Factor / Q000008:administration & dosage; D013482:Superoxide Dismutase / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D019210:Troponin I / Q000097:blood / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000378:metabolism; D018754:Ventricular Dysfunction / Q000188:drug therapy
chemical_list: D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D051197:Toll-Like Receptor 4; D019210:Troponin I; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D045022:Lactate Dehydrogenases; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D052279:Creatine Kinase, MB Form; D000068800:Etanercept