Beneficial effects of growth hormone-releasing peptide on myocardial oxidative stress and left ventricular dysfunction in dilated cardiomyopathic hamsters.
Kato. Yosuke Y; Iwase. Mitsunori M; Ichihara. Sahoko S; Kanazawa. Hiroaki H; Hashimoto. Katsunori K; Noda. Akiko A; Nagata. Kohzo K; Koike. Yasuo Y; Yokota. Mitsuhiro M
Key Findings
- GHRP‑2 (1 mg/kg) reduced left‑ventricular dilation and wall thinning in diseased hamsters.
- Treatment lowered myocardial fibrosis compared with untreated controls.
- GHRP‑2 prevented the drop in the GSH/GSSG antioxidant ratio and the rise in 4‑HNE, markers of oxidative stress.
Practical Outcomes
- The study suggests GHRP‑2 might have heart‑protective effects by cutting oxidative stress, but it’s an animal experiment, not a human trial. For biohackers, it’s an interesting hint that GHRP‑2 could support cardiac health, yet there’s no proven dosing or safety data for people, so it shouldn’t be added to a regimen without further evidence.
Summary
In a hamster model of dilated cardiomyopathy, giving the peptide GHRP‑2 reduced heart oxidative damage and slowed the worsening of heart size and function. The peptide helped keep the heart's antioxidant balance healthier and lowered harmful lipid‑peroxidation products.
Abstract
Growth hormone-releasing peptide (GHRP) may act directly on the myocardium and improve left ventricular (LV) function, suggesting a potential new approach to the treatment of cardiomyopathic hearts. The present study tested the hypothesis that the beneficial cardiac effects of GHRP might include attenuation of myocardial oxidative stress. Dilated cardiomyopathic TO-2 hamsters were injected with GHRP-2 (1 mg/kg) or saline from 6 to 12 weeks of age. F1B hamsters served as controls. Untreated TO-2 hamsters progressively developed LV dilation, wall thinning, and systolic dysfunction between 6 and 12 weeks of age. Marked myocardial fibrosis was apparent in untreated hamsters at 12 weeks of age in comparison with F1B controls. The ratio of reduced to oxidized glutathione (GSH/GSSG) was decreased and the concentration of 4-hydroxynonenal (4-HNE) was increased in the hearts of untreated TO-2 hamsters. Treatment with GHRP-2 attenuated the progression of LV remodeling and dysfunction, as well as myocardial fibrosis, in TO-2 hamsters. GHRP-2 also inhibited both the decrease in the GSH/GSSG ratio and the increase in the concentration of 4-HNE in the hearts of TO-2 hamsters. GHRP-2 can suppress the increase in the level of myocardial oxidative stress, leading to attenuation of progressive LV remodeling and dysfunction in dilated cardiomyopathic hamsters. (Circ J 2010; 74: 163 - 170).
Study Information
pubmed
2009
2009-11-27T00:00:00.000Z
10.1253/circj.cj-09-0378