Protective effect of melanocortin peptides in rat myocardial ischemia.
Bazzani. C C; Guarini. S S; Botticelli. A R AR; Zaffe. D D; Tomasi. A A; Bini. A A; Cainazzo. M M MM; Ferrazza. G G; Mioni. C C; Bertolini. A A
Key Findings
- ACTH-(1-24) lowered arrhythmias and death after brief heart blockage in a dose‑dependent way
- High dose ACTH prevented the rise in blood free radicals after reperfusion
- NDP‑MSH increased the amount of healthy heart tissue after a permanent blockage
Practical Outcomes
- The data hint that melanocortin peptides could protect the heart, which is interesting for longevity‑focused biohackers, but the results are from rats and use high intravenous or sub‑cutaneous doses. No human safety or dosing info exists, so it’s not ready for self‑experimentation; it mainly signals a research direction rather than a usable protocol.
Summary
In rats, giving melanocortin peptides (similar to the skin‑tanning peptide melanotan‑I) right after a heart attack reduced dangerous heart rhythms, lowered death rates, cut the spike in harmful free radicals, and helped more heart tissue stay healthy. The effect was stronger with higher doses, but the study was done only in animals, not people.
Abstract
The influence of the melanocortin peptide ACTH-(1-24) (adrenocorticotropin) on the consequences of short-term coronary ischemia (5 min) followed by reperfusion, and the effect of the long-acting melanocortin [Nle(4),D-Phe(7)]alpha-melanocyte-stimulating hormone (NDP-MSH) on the damage induced by a permanent coronary occlusion, were investigated in anesthetized rats. Ischemia was produced by ligature of the left anterior descending coronary artery. Reperfusion-induced arrhythmias [ventricular tachycardia (VT), ventricular fibrillation (VF)] and survival rate within the 5 min following reperfusion, blood levels of free radicals detected 2 min after reperfusion by electron spin resonance spectrometry, and amount of healthy myocardial tissue, measured 72 h after permanent coronary occlusion on immunohistologically stained serial sections, were evaluated. Postischemic reperfusion induced VT in all saline-treated rats, and VF and death in a high percentage of animals (87%). In rats treated i.v. (2.5 min after coronary occlusion) with ACTH-(1-24) (0.16-0.48 mg/kg) there was a significantly dose-dependent reduction in the incidence of arrhythmias and lethality. Ischemia/reperfusion caused a large increase in free radical blood levels; treatment with ACTH-(1-24) (0.48 mg/kg i.v.) almost completely prevented this increase. In rats subjected to permanent coronary occlusion, the amount of healthy myocardial tissue was much reduced in saline-treated rats, while in rats treated s.c. with NDP-MSH (0.27 mg/kg every 12 h) it was significantly higher. The present data demonstrate, for the first time, an unforeseen property of melanocortin peptides, i.e., their ability to significantly reduce both heart ischemia/reperfusion injury and size of the ischemic area induced by permanent coronary occlusion.
Study Information
pubmed
2001