Study summary · research use only
Modulation of PTEN by hexarelin attenuates coronary artery ligation-induced heart failure in rats
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study, the authors examined whether hexarelin, a synthetic growth hormone-releasing peptide, is associated with changes in heart failure (HF) induced by permanent coronary artery ligation (CAL). Rats were divided into control, sham, hexarelin-treated HF, and untreated HF groups and given subcutaneous hexarelin (100 mcg/kg) or saline twice daily for 30 days, with assessment of left ventricular function, oxidative stress, apoptosis, and cardiac structure. Hexarelin treatment was associated with upregulation of phosphatase and tensin homologue (PTEN) expression, reduced phosphorylation of Akt and mTOR, improved left ventricular function measures, reduced myocardial remodeling, and reduced oxidative stress markers, compared with untreated HF rats. The authors describe these findings as indicating an association between PTEN upregulation, reduced Akt/mTOR signaling, and CAL-induced HF outcomes.
Abstract
Hexarelin is a synthetic growth hormone-releasing peptide that exerts cardioprotective effects. However, its cardioprotective effect against heart failure (HF) is yet to be explained. This study investigated the therapeutic role of hexarelin and the mechanisms underlying its cardioprotective effects against coronary artery ligation (CAL)-induced HF in rats. Rats with four weeks of permanent CAL, induced myocardial infarction, and HF were randomly separated into four groups: the control group (Ctrl), sham group (Sham), hexarelin treatment group (HF + Hx), and heart failure group (HF). The rats were treated with subcutaneous injection of hexarelin (100 μg/kg) in the treatment group or saline in the other groups twice a day for 30 days. Left ventricular (LV) function, oxidative stress, apoptosis, molecular analyses, and cardiac structural and pathological changes in rats were assessed. The treatment of HF rats with hexarelin significantly induced the upregulation of phosphatase and tensin homologue (PTEN) expression and inhibited the phosphorylation of protein kinase B (Akt) and mammalian target of rapamycin (mTOR) to significantly improve LV function, ameliorate myocardial remodeling, and reduce oxidative stress. These findings indicate that hexarelin attenuates CAL-induced HF in rats by ameliorating myocardial remodeling, LV dysfunction, and oxidative stress via the upmodulation of PTEN signaling and downregulation of the Akt/mTOR signaling pathway.
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