Potent mitochondria-targeted peptides reduce myocardial infarction in rats
Abstract
OBJECTIVE: Previously, we demonstrated that a novel opiate peptide, 2',6'-dimethyl-tyrosine-D-Arg-Phe-Lys-NH2, provided cardioprotection against myocardial stunning in vivo. We subsequently showed that this peptide targeted mitochondria and can scavenge reactive oxygen species. The objective of this study was to determine the role of opioid versus antioxidant activity in cardioprotection. METHODS: We compared two mitochondria-targeted peptide analogs that lacked opioid activity: SS-31 (D-Arg-2',6'-dimethyl-tyrosine-Lys-Phe-NH2) and SS-20 (Phe-D-Arg-Phe-Lys-NH2). They differ in that only SS-31 has scavenging ability. Rats (n=8/group) were randomized to SS-31, SS-20 or placebo. The drugs (3 mg/kg) or saline was administered intraperitoneally 30 min before ligation of the left anterior descending artery for 60 min, and another dose given intraperitoneally 5 min before reperfusion for 60 min. Study endpoints included myocardial infarct size, cardiac arrhythmia and myocardial lipid peroxidation. RESULTS: The area at risk was similar among the groups. The infarct area/area at risk, however, was significantly smaller in the treatment groups (53.9+/-1.1% in SS-31 group, 47.1+/-1.4% in SS-20 group, versus 59.9+/-1% in the controls, P<0.01). Lipid peroxidation was significantly reduced by both SS-31 and SS-20 treatment. Arrhythmia occurred only during the early period of coronary occlusion and was less frequent and less severe in the peptide treatment groups than in the controls (Lambeth score 5 points, 3 points, versus 13 points in the controls, P<0.05). CONCLUSIONS: This study shows that pretreatment with both SS-31 and SS-20 significantly reduced myocardial lipid peroxidation and infarct size in ischemia-reperfusion injury, and suggests that the cardioprotective properties of 2',6'-dimethyl-tyrosine-D-Arg-Phe-Lys-NH2 was primarily mediated by its antioxidant properties. As SS-20 does not scavenge reactive oxygen species, it most likely reduces reactive oxygen species production during ischemia-reperfusion.
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SS-31 is effective against myocardial ischemia-reperfusion injury in both ex vivo and in vivo models.
“It is also effective against myocardial ischemia-reperfusion injury in both ex vivo and in vivo models176, 179.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [179]
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Targeted Antioxidants in Exercise-Induced Mitochondrial Oxidative Stress: Emphasis on DNA Damage
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Systems biology of antioxidants
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Mitochondrial Membrane Permeability Inhibitors in Acute Myocardial Infarction
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- Authors
- Cho, J., Won, K., Wu, D., Soong, Y., Liu, S., Szeto, H. H., & Hong, M. K.
- Affiliations
- Cornell University (US)
- Weill Cornell Medicine (US)
- St. Luke's-Roosevelt Hospital Center (US)
- Corresponding author
- Cho, Janghyun
- Szeto, Hazel H.
- Hong, Mun K.
- Venue
- Coronary Artery Disease
- Published
- 2007-05
- Volume
- 18
- Issue
- 3
- Pages
- 215-220
- ISSN
- 0954-6928 (ISSN-L)
- OpenAlex
- W2003139013
- Cited by
- 144
- References
- 18
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 1 · 2023: 4 · 2022: 8 · 2021: 7 · 2020: 12 · 2019: 9 · 2018: 7 · 2017: 11 · 2016: 7 · 2015: 6 · 2014: 9 · 2013: 15 · 2012: 14
- FWCI
- 3.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Coronary Artery Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Drug Abuse (P01 DA 08924, P01DA008924)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Keywords
- SS-31, mitochondria-targeted peptide, myocardial infarction, cardioprotection, ischemia-reperfusion injury, reactive oxygen species scavenging, lipid peroxidation, cardiac arrhythmias, opioid peptides, myocardial stunning
- MeSH terms
- Animals, Antioxidants, Male, Mitochondria, Myocardial Infarction, Oligopeptides, Lipid Peroxidation, Myocardial Reperfusion, Rats, Sprague-Dawley, Reactive Oxygen Species, Rats
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