GHRP-6 has demonstrated exceptional benefits for liver health, particularly in preventing and reducing liver fibrosis.
In addition to its cytoprotective effects, growth hormone-releasing peptide 6 (GHRP-6) proved to reduce liver fibrotic induration.
Tissue fibrosis is a leading cause of morbidity and mortality. Current treatments for conditions such as hepatic fibrosis have been unsuccessful. The growth hormone releasing peptide 6 (GHRP6) is endowed with cardioprotective actions but its antifibrotic effect had not been anticipated. We examined the GHRP6 ability to prevent and revert liver cirrhosis after induction in Wistar rats by a subcutaneous administration of CCl4.
GHRP6 attenuates hypoxia damage in the liver, which is considered the main limitation for successful hepatic transplantation. Additionally, GHRP6 attenuates the MOD syndrome resulting from the systemic inflammatory response during hepatic reperfusion, protecting remote organs that had not been previously tested such as: small intestine, lungs and kidneys.
In addition to focal necrosis, perivascular fibrotic induration was another hepatic change attributable to Dox cumulative toxicity and evidenced in the saline group. Interestingly, no evidences of pathologic fibrotic induration were ever detected in the liver of rats receiving GHRP-6.
GHRP-6 intervention showed to rescue from coagulative necrosis a variety of epithelial cells as hepatocytes, kidneys tubular cells, bronchial epithelia, and the jejunum-ileum enterocytes.
Liver congestion in saline group was classified as evident-to-severe versus less than mild congestion for the GHRP-6 group. In line with this, ALAT circulating levels were also significantly higher in the saline group than in rats receiving GHRP-6.
In vivo studies showed that, compared with baseline values, ischaemia/reperfusion caused marked hepatic and intestinal damage, neutrophilic infiltration and lipid peroxidation. Pre-treatment with GHRP-6 alone truncated these effects by 50-85% and an additional benefit was seen when GHRP-6 was used in combination with EGF. Lung and renal injuries were also reduced by these pre-treatments.
Anti-fibrotic: via upregulation of PPARγ, which is followed by a transforming growth factor-beta (TGF-β), CTGF, and platelet-derived growth factor (PDGF) downregulation. Anti-inflammatory: blunts NFκB expression and activation.
