GHRP-6 demonstrates exceptional benefits for tissue healing and regeneration through multiple complementary mechanisms.
In addition to its cytoprotective effects, growth hormone-releasing peptide 6 (GHRP-6) proved to reduce liver fibrotic induration. CD36 as one of the GHRP-6 receptors appears abundantly represented in cutaneous wounds granulation tissue.
The experiment in rats, based on clean full-thickness controlled wounds, indicated that GHRP-6 pharmacodynamics has likely involved attenuation of immunoinflammatory mediators, their effector cells, and the reduction of fibrosis-inducing cytokines. The concerted action of these two elemental mechanisms may have theoretically translated into a particular modulation of fibroblasts response to injury, leading to precocious closure with a reduced scarring. Outstandingly, the mechanisms underlying this pattern of healing do not appear to interfere with the angiogenic repopulation nor with the reepithelialization process.
This antiscar effect was explained by interfering with TGF-β-dependent activation of myofibroblasts differentiation and reduction of ECM proteins accumulation. Similarly, antiscarring healing properties are described for plants’ principles that downregulate the expression of fibrogenic-related molecules such as TGF-β1 and the downstream events, leading to fibrosis and scar formation. In addition to a direct action of GHRP-6 on TGFB1 gene expression, we deem that the reduction of inflammatory effectors could have also contributed to enhancing the healing process and to reducing fibrosis.
An important contribution is the unprecedented evidence that the peptide reduced the onset of HTS in the rabbit’s ear model. This represents an extension of the GHRP-6 antifibrotic potential demonstrated years ago by our group in an animal model of liver fibrosis.
Two relevant effects were displayed by GHRP-6 intervention in the realm of Dox-derived toxicity: the broad cytoprotective responses induced by the peptide in different internal epithelial organs, and the anti-fibrotic response detected in both liver and kidney parenchyma. 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.
Beyond its role in muscle building, GHRP-6 also enhances connective tissue repair and supports the healing of tendons, ligaments, and joints. This is due in part to GH’s ability to promote collagen synthesis and angiogenesis (formation of new blood vessels), which are essential for tissue regeneration.
In addition to upregulating IGF-1 expression, the GHRP-6 biotin conjugate treatment also stimulated the synthesis of collagen type I proteins in cultured C2C12 cells. While the exact role of extracellular matrix molecules in myogenesis is not yet fully understood, previous studies have reported that collagen may be involved in satellite cell self-renewal, muscle regeneration, muscle differentiation, and wound healing. Recently, Zhou et al reported that collagen synthesis significantly increases during wound healing in muscle tissue after surgery.
