GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Growth hormone-releasing peptide-6 inhibits cerebellar cell death in aged rats.
Pañeda. Covadonga C; Arroba. Ana I AI; Frago. Laura M LM; Holm. Anne Mette AM; Rømer. John J; Argente. Jesús J; Chowen. Julie A JA
Key Findings
- Aged rats have lower IGF‑I mRNA in the cerebellum and higher activation of death‑related caspases 3 and 9.
- GHRP‑6 treatment restores IGF‑I mRNA levels in the aged cerebellum.
- GHRP‑6 reduces neuronal cell death and suppresses caspase 3 and 9 activation in aged rats.
Practical Outcomes
- The study hints that GHRP‑6 could have neuroprotective effects by boosting IGF‑1 and blocking cell‑death pathways, which may be of interest for longevity or brain‑health protocols. However, the data are limited to rats, with no human dosing or safety information, so any real‑world use would be experimental and should be approached with caution.
Summary
In older rats, the brain's cerebellum makes less IGF‑1, a protein that helps nerve cells survive, and more cells die. Giving the peptide GHRP‑6 raised IGF‑1 messenger levels, cut down cell death, and blocked the enzymes (caspases) that trigger dying. This suggests GHRP‑6 might protect aging brain cells, at least in rats.
Abstract
Insulin-like growth factor (IGF)-I is essential for cerebellar granule neuron survival and a decline in IGF-I is implicated in various age-dependent processes. Here we show that IGF-I mRNA levels are decreased in the cerebellum of old rats compared with young rats and this was associated with increased cell death and activation of caspases 3 and 9. Growth hormone-releasing peptide (GHRP)-6, a synthetic ligand for the ghrelin receptor, increased IGF-I mRNA levels, decreased cell death and inhibited caspase 3 and 9 activation in the cerebellum of aged rats. These results suggest that increasing IGF-I expression in the cerebellum can decrease cell death in aged rats via inhibition of caspase 3 and 9 activation.
Study Information
pubmed
2003
2003-08-26T00:00:00.000Z
10.1097/00001756-200308260-00018
25
20