GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Effect of exogenous ghrelin on cell differentiation antigen 40 expression in endothelial cells.
Zhang. Min M; Yuan. Fang F; Chen. Hui H; Qiu. Xingbiao X; Fang. Weiyi W
Key Findings
- Exogenous ghrelin dramatically lowers CD40 mRNA and protein levels in endothelial cells (up to ~77% reduction at 1000 ng/ml).
- The anti‑inflammatory effect is dose‑dependent and is blocked by the GHSR antagonist [d‑Lys]-GHRP‑6, indicating it works through the GHSR‑1a receptor.
- Des‑acyl ghrelin does not inhibit CD40 expression, highlighting that only the active ghrelin form has this effect.
Practical Outcomes
- For biohackers, the data suggest that ghrelin (or ghrelin‑releasing peptides) might help reduce vascular inflammation, but the benefit can be negated by GHRP‑6 antagonists. It reinforces using active ghrelin‑based compounds rather than des‑acyl forms for anti‑inflammatory goals, though human dosing and safety remain untested.
Summary
The study shows that giving ghrelin (the hormone that also triggers growth hormone release) to human vein cells cuts down a key inflammation marker called CD40. This effect depends on the amount of ghrelin and works through its main receptor, GHSR‑1a. A ghrelin‑blocking peptide, [d‑Lys]-GHRP‑6, reduces this benefit, while the inactive form of ghrelin (des‑acyl ghrelin) does nothing.
Abstract
Ghrelin is a brain-gut peptide that serves as a natural ligand for growth hormone secretagogue receptor (GHSR). It also exists abundantly in the cardiovascular system. In order to evaluate the possible role of ghrelin in the development of atherosclerosis, the effect of ghrelin on the expression of cell differentiation antigen 40 (CD40) were studied. Human umbilical vein endothelial cell (HUVEC) line-ECV 304 was pre-treated with different concentrations of ghrelin, des-acyl ghrelin or [d-Lys]-GHRP-6 (a ghrelin receptor antagonist), and then induced with tumor necrosis factor-alpha (TNF-alpha) and interferon gamma (IFN-gamma). The mRNA levels of CD40 were analyzed by reverse transcription-polymerase chain reaction, and the expressions of CD40 protein in the cells were measured by flow cytometry (FCM) and Western blotting. The results showed that exogenous ghrelin could significantly inhibit TNF-alpha/IFN-gamma induced CD40 expression in HUVEC cells in a concentration-dependent manner. When treated with 1000 ng/ml of ghrelin, the mRNA level of CD40 in the cells was decreased by approximately 77%, but when treated with both 1000 ng/ml of ghrelin and 1000 ng/ml of [d-Lys]-GHRP-6, the mRNA level of CD40 in the cells was decreased by only 42%, suggesting that [d-Lys]-GHRP-6 could counteract the inhibitory effect of ghrelin in these cells. However, CD40 expression was not inhibited by des-acyl ghrelin at 1000 ng/ml. The results in protein expression analysis detected by FCM and Western blotting further confirmed these results. Our results suggested that in the cardiovascular system, ghrelin not only has an anti-inflammatory effect, but also has a significant immunoregulatory effect that may be mediated through the GHSR-1a receptor.
Study Information
pubmed
2007
10.1111/j.1745-7270.2007.00365.x