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ORIGINAL ARTICLE
Year : 2021  |  Volume : 64  |  Issue : 6  |  Page : 281-288

A study of the cardioprotective effect of spermidine: A novel inducer of autophagy


1 Department of Medical Physiology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt
2 Department of Medical Biochemistry, Faculty of Medicine, University of Alexandria, Alexandria, Egypt
3 Department of Clinical Pharmacology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt

Correspondence Address:
Dr. Eman Magdy Omar
Department of Medical Physiology, Faculty of Medicine, Al-Mowassat Hospital, Alexandria University, Alexandria
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cjp.cjp_76_21

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Acute myocardial infarction (AMI) is an instant death of cardiomyocytes that ends in a large mortality worldwide. Thus, there is a great interest to come up with novel protective approaches for AMI to mount cardiomyocyte survival, enhance postinfarcted cardiac function, and countermand the process of cardiac remodeling. Spermidine has vital roles in vast cellular processes under pathophysiological circumstances. This study aims to enhance our comprehension of the role of autophagy as a possible protective sequel of spermidine supplementation on postinfarction ventricular dysfunction in a rat model of AMI induced by isoproterenol (ISO). Thirty male rats were divided into three groups (control, AMI, and spermidine + AMI). AMI was induced by subcutaneous ISO injections for two consecutive days. Rats were pretreated with spermidine by intraperitoneal injection before induction of AMI. Electrocardiogram (ECG) was recorded in all rats 24 h after the second dose of ISO. Rats were sacrificed after ECG recording, and samples were taken for biochemical assessments. Spermidine intake before induction of AMI in rats significantly attenuated cardiac dysfunction where cardiac enzymes are decreased, and ECG changes induced by ISO are reversed in cardiomyocytes. Spermidine affects the autophagic flux of autophagy-related protein expression (LC3-II, TFEP, and p62). Furthermore, it increased the total antioxidant capacity.


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