Literature DB >> 23054911

The effect of c-fos on acute myocardial infarction and the significance of metoprolol intervention in a rat model.

Song Zhang1, Meiqi Zhang, Steven Goldstein, Yigang Li, Junbo Ge, Ben He, George Ruiz.   

Abstract

Over-expression of c-fos may play a role in some diseases. Research pertaining to the expression of c-fos in acute myocardial ınfarction (AMI) is rare, and the detailed role of c-fos in AMI has not been reported. Therefore, the purpose of this project was to elucidate the detailed effect of c-fos on AMI rats and evaluate the effect of a metoprolol intervention. An AMI rat model was established for the purposes of this study. The expression of c-fos in AMI was evaluated via immunohistochemical analysis and in situ hybridization. Simultaneously, we investigated the effect of c-fos on AMI rats via medicinal treatment with c-fos monoclonal antibody, isoproterenol, and metoprolol. Positive c-Fos protein expression and c-fos mRNA expression in cardiomyocytes were increased at 1, 3, 7, and 10 days after ligation in AMI rats compared with a sham-operated group. Peak expression occurred at 3 days after ligation. The weight percentage fraction of infarct size was decreased in rats treated with c-fos monoclonal antibody compared with the control normal saline treatment group. The weight percentage fraction of infarction size was increased after c-fos was increased via the administration of isoproterenol. c-Fos protein expression and the infarct size in rats treated with metoprolol were also decreased compared with the control normal saline treatment group. The results showed that c-fos expression rapidly increased after coronary ligation; c-fos plays an important role in myocardial lesions and is likely to be involved in the pathogenesis of AMI as well. Metoprolol can inhibit the expression of c-fos and has a positive therapeutic effect on rats after AMI; the involvement effect of metoprolol on myocardial infarction might be correlated with its effect on the inhibition of c-fos.

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Year:  2013        PMID: 23054911     DOI: 10.1007/s12013-012-9428-0

Source DB:  PubMed          Journal:  Cell Biochem Biophys        ISSN: 1085-9195            Impact factor:   2.194


  9 in total

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8.  Novel p38 Mitogen-Activated Protein Kinase Inhibitor Reverses Hypoxia-Induced Pulmonary Arterial Hypertension in Rats.

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9.  Metoprolol Mitigates Ischemic Heart Remodeling and Fibrosis by Increasing the Expression of AKAP5 in Ischemic Heart.

Authors:  Feng Zhu; Qiushu Wang; Zhi Wang; Xu Zhang; Benkai Zhang; Hegui Wang
Journal:  Oxid Med Cell Longev       Date:  2022-10-04       Impact factor: 7.310

  9 in total

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