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Nesfatin-1 Attenuates Injury in a Rat Model of Myocardial Infarction by Targeting Autophagy, Inflammation, and Apoptosis Publisher Pubmed



Naseroleslami M1 ; Sharifi M2, 3 ; Rakhshan K4 ; Mokhtari B2, 3 ; Aboutaleb N2, 3
Authors
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Authors Affiliations
  1. 1. Department of Cellular and Molecular Biology, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
  2. 2. Physiology Research Center, Iran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Physiology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Source: Archives of Physiology and Biochemistry Published:2023


Abstract

Nesfatin-1 plays an important role in the modulation of heart performance. However, it remains unclear how nesfatin-1 contributes to cell survival in acute myocardial infarction (MI). A rat model of MI was established via ligation of left anterior descending coronary artery (LAD) for 30 min and 20 µg/kg concentration of nesfatin-1 was intraperitoneally infused prior to reperfusion. At 24 h after reperfusion, oxidative stress markers, the expression of caspase3, beclin-1, pro-inflammatory cytokines, and the mRNA levels of Bax and Bcl-2 were evaluated. Results showed that nesfatin-1 markedly restored GSH content and SOD activity as well as reduced MDA levels compared to only the MI group (p <.05). Likewise, nesfatin-1 contributed to cell survival by inhibiting autophagy and apoptosis markers such as caspase3 and Bax (p <.05). Collectively, these findings support the idea that nasfatin-1 can be used as a good candidate to treat MI by targeting oxidative stress, apoptosis, and autophagy. © 2020 Informa UK Limited, trading as Taylor & Francis Group.