title: Cardiovascular protective effects of IL-1 ra-Fc-IL-18BP on experimental myocardial infarction by inhibiting oxidative stress and inflammation in a rat model.
abstract: In this study, we examined the cardiovascular protective effects of IL-1ra-Fc-IL-18BP on experimental myocardial infarction in a rat model. An animal model of myocardial infarction (MI) was induced by permanent ligation of the left anterior descending coronary artery (LAD) in SD rats. After surgery sixty male rats and sixty female rats were randomly divided into groups as followed: sham group, MI group, IL-1ra-Fc-IL-18BP 50,100, 200 mg/kg treatment groups, and verapamil 5 mg/kg treatment group. IL-1 ra-Fc-IL-18BP and verapamil were administered to the animals immediately after operation by intravenous injection. Treatment with IL-1ra-Fc-IL-18BP (50, 100 and 200 mg/kg) could remarkably decrease infarct size from 24.82% to 13.43% (p < 0.05), and decrease the activities of serum aspartate aminotransferase (AST), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) compared with sham group (p < 0.05). Meanwhile, treatment with IL-1ra-Fc-IL-18BP (200 mg/kg) could significantly increase the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), but decreased the content of malondiadehyde (MDA) in serum (p < 0.05). Furthermore, IL-1ra-Fc-IL-18BP marablely reduced the content of calcium (Ca2+) in serum (p < 0.05), and also decreased the levels of serum interleukin-1β (IL-1β), tumor necrosis factor (TNF-α) (p < 0.05). Histopathological results demonstrated the same protective effect of IL-1ra-Fc-IL-18BP All these results above indicated that IL-1ra-Fc-IL-18BP has protective effects in myocardial infarction, improves free radicals metabolism, ameliorates myocardial calcium overload and inhibits the release of inflammatory cytokines.
authors.forename: Hong
authors.initials: H
authors.lastname: Zhang
authors.forename: Huali
authors.initials: H
authors.lastname: Xu
authors.forename: Haolin
authors.initials: H
authors.lastname: Xie
authors.forename: Feng
authors.initials: F
authors.lastname: Li
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Yu
authors.forename: Dayun
authors.initials: D
authors.lastname: Sui
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002118:Calcium / Q000097:blood; D002316:Cardiotonic Agents / Q000494:pharmacology*; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins / Q000494:pharmacology*; D053590:Interleukin 1 Receptor Antagonist Protein / Q000494:pharmacology*; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011993:Recombinant Fusion Proteins / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D002316:Cardiotonic Agents; D016207:Cytokines; C000592496:IL-1ra-Fc-IL-18bp fusion protein; D036341:Intercellular Signaling Peptides and Proteins; D053590:Interleukin 1 Receptor Antagonist Protein; D011993:Recombinant Fusion Proteins; D002118:Calcium