GH-releasing peptide-2 administration prevents liver inflammatory response in endotoxemia.
Granado. Miriam M; Martín. Ana Isabel AI; López-Menduiña. María M; López-Calderón. Asunción A; Villanúa. M Angeles MA
Key Findings
- GHRP-2 reduced LPS‑induced spikes in blood transaminases (liver damage markers).
- It lowered circulating nitrites/nitrates and hepatic TNF‑alpha while raising IGF‑I mRNA in the liver.
- The protective effect required non‑parenchymal liver cells; isolated hepatocytes did not show the benefit.
Practical Outcomes
- For biohackers, this suggests GHRP‑2 might have anti‑inflammatory and liver‑protective properties beyond its growth‑hormone effects, especially in situations of acute stress or endotoxin exposure. However, the data are from a rat model with high doses and no human trials, so any protocol would be experimental and should be approached cautiously, ideally after consulting medical expertise.
Summary
In rats given a bacterial toxin that normally hurts the liver, the peptide GHRP-2 (a ghrelin‑like compound) lowered liver enzymes, reduced harmful nitric oxide, cut down inflammatory TNF‑alpha, and boosted IGF‑I levels, indicating it protected the liver. The effect seemed to come from actions on liver support cells rather than the liver cells themselves.
Abstract
It has been reported that growth hormone (GH)-releasing peptide-2 (GHRP-2), a ghrelin receptor agonist, has an anti-inflammatory effect. We investigated whether this GH secretagogue attenuates liver injury in LPS-treated rats. Wistar rats were simultaneously injected (ip) with LPS (1 mg/kg) and/or GHRP-2 (100 microg/kg). Serum levels of aspartate and alanine transaminases were measured as an index of liver damage. Circulating nitrites/nitrates and hepatic IGF-I and TNF-alpha were evaluated as possible mediators of GHRP-2 actions. LPS increased serum levels of transaminases and nitrites/nitrates. Moreover, LPS increased hepatic TNF-alpha and decreased hepatic IGF-I mRNAs. GHRP-2 administration attenuated the effects of LPS on transaminases, nitrites/nitrates, TNF-alpha, and IGF-I in vivo. This GHRP-2 effect does not seem to be due to modifications in food intake, since fasting did not modify serum levels of transaminases, serum nitrites/nitrates, and hepatic TNF-alpha mRNA both in vehicle rats and in LPS-injected rats. To elucidate whether GHRP-2 is acting directly on the liver, cocultures of hepatocytes and nonparenchymal cells and monocultures of isolated hepatocytes were incubated with LPS and GHRP-2. The ghrelin receptor agonist prevented an endotoxin-induced increase in transaminases and nitrite/nitrate release as well as in TNF-alpha mRNA and increased IGF-I mRNA from cocultures of hepatocytes and nonparenchymal cells, but not from monocultures. In summary, these data indicate that GHRP-2 has a protective effect on the liver in LPS-injected rats that seems to be mediated by IGF-I, TNF-alpha, and nitric oxide. Our data also suggest that the anti-inflammatory effect of GHRP-2 in the liver is exerted on nonparenchymal cells.
Study Information
pubmed
2007
2007-11-06T00:00:00.000Z
10.1152/ajpendo.00308.2007