Growth Hormone-Releasing Peptide-6 (GHRP-6) Ameliorates Post-Infarct Ventricular Remodeling and Systolic Dysfunction in a Model of Permanent Coronary Ligation.
GHRP-6 may have cardioprotective effects in a rat model of myocardial infarction, but further research is needed to determine its relevance to human health.
Where it sits
this study against the rest of the hexarelin corpusSummary and findings
This study investigated the effects of GHRP-6 on post-infarct ventricular remodeling and systolic dysfunction in a rat model of permanent coronary artery ligation. The treatment was administered at a dose of 0.4 mg/kg for 7 days following surgery. Results indicated improvements in myocardial tissue integrity and left ventricle physiology.
Abstract
<b>Background/Objective</b>: GHRP-6 is a GH secretagogue hexapeptide with expanding and promising cardioprotective effects. Having determined 0.4 mg/kg as the minimum effective dose for enhancing inotropy based on echocardiographic parameters in healthy rats, we implemented a non-reperfusion myocardial infarct model, with its consequent left ventricle wall thinning and ballooning, via permanent left descending coronary artery ligation. <b>Methods</b>: Rats were assigned to three groups: sham-operated/normal rats, infarcted + saline-treated control rats, and infarcted + GHRP-6-administration rats. Treatments were initiated post-surgery and continued for 7 days. On day 7, the animals were echocardiographically and histologically evaluated. For mitochondrial proteomic analysis, an additional 12 healthy rats were used. Six animals received GHRP-6 or normal saline and were observed for 6 h after the inoculation. <b>Results</b>: Here, we show that GHRP-6 attenuated myocardial tissue demise, reduced myocardial interstitial fibrosis/scarring, and integrally improved left ventricle physiology. The proteomic analysis indicated that the GHRP-6 cardioprotective effects may be theoretically mediated by the concerted upregulation of proteins/pathways involved in fatty acid beta-oxidation, apoptosis prevention pathways, antioxidant defenses, and mitochondrial metabolic reprogramming. <b>Conclusions</b>: GHRP-6 is a potent cardioprotective candidate attenuating morphological and functional outcomes caused by late ischemia.