GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Acylated Ghrelin Attenuates l-Thyroxin-induced Cardiac Damage in Rats by Antioxidant and Anti-inflammatory Effects and Downregulating Components of the Cardiac Renin-angiotensin System.
Badi. Rehab R
Key Findings
- Acylated ghrelin (AG) reduces cardiac hypertrophy and damage caused by excess thyroid hormone in rats.
- AG improves antioxidant defenses (SOD2, GSH), reduces oxidative stress markers, and lowers inflammatory cytokines (TNF‑α, IL‑6).
Practical Outcomes
- For biohackers, the study hints that activating the ghrelin receptor (e.g., with GHRP‑6) could offer heart‑protective antioxidant and anti‑inflammatory benefits, especially under stress or hormonal imbalance. However, the research is in rats, uses a disease model, and provides no human dosing guidance, so any protocol would be experimental and should be approached with caution.
Summary
In rats with too much thyroid hormone, giving the hormone ghrelin (the active form) helped protect the heart. It did this by boosting antioxidant enzymes, lowering inflammation, and calming down a heart‑related hormone system. When a drug that blocks the ghrelin receptor (a modified GHRP‑6) was added, all the benefits disappeared, showing the receptor is key for the protection.
Abstract
This study investigated the protective effect of acylated ghrelin (AG) against l-thyroxin (l-Thy)-induced cardiac damage in rats and examined possible mechanisms. Male rats were divided into five intervention groups of 12 rats/group: control, control + AG, l-Thy, l-Thy + AG, and l-Thy + AG + [D-Lys3]-GHRP-6 (AG antagonist). l-Thy significantly reduced the levels of AG and des-acyl ghrelin and the AG to des-acyl ghrelin ratio. Administration of AG to l-Thy-treated rats reduced cardiac weights and levels of reactive oxygen species and preserved the function and structure of the left ventricle. In addition, AG also reduced the protein levels of cleaved caspase-3 and cytochrome c and prevented mitochondrial permeability transition pore opening. In the left ventricle of both control + AG-treated and l-Thy + AG-treated rats, AG significantly increased left ventricular levels of manganese superoxide dismutase (SOD2), total glutathione (GSH), and Bcl2. It also reduced the levels of malondialdehyde, tumor necrosis factor-α (TNF-α), interleukin-6, and Bax and the nuclear activity of nuclear factor-kappa B. Concomitantly, in both treated groups, AG reduced the mRNA and protein levels of NADPH oxidase 1, angiotensin (Ang) II type 1 receptor, and Ang-converting enzyme 2. All the beneficial effects of AG in l-Thy-treated rats were prevented by the coadministration of [D-Lys3]-GHRP-6, a selective growth hormone secretagogue receptor subtype 1a antagonist. In conclusion, AG protects against hyperthyroidism-induced cardiac hypertrophy and damage, which is mainly due to its antioxidant and anti-inflammatory potentials and requires the activation of GHS-R1a.
Study Information
pubmed
2021
2021-09-01T00:00:00.000Z
10.1097/fjc.0000000000001084