Study summary · research use only
The tri-peptide GHK-Cu complex ameliorates lipopolysaccharide-induced acute lung injury in mice
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study examined the tripeptide-copper complex glycyl-l-histidyl-l-lysine-Cu (II) (GHK-Cu) using lipopolysaccharide (LPS)-stimulated RAW 264.7 mouse macrophages in vitro and a mouse model of acute lung injury (ALI) in vivo. The abstract reports that GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity, and decreased TNF-α and IL-6 production, associated with suppression of NF-κB p65 and p38 MAPK signaling in both settings. GHK-Cu was also reported to lessen LPS-induced lung histological changes and reduce infiltration of inflammatory cells into lung tissue in mice. The authors describe GHK-Cu as having a protective effect in this LPS-induced ALI model, and suggest it may represent an approach for ALI/acute respiratory distress syndrome (ARDS), pending further research.
Abstract
The tripeptide-copper complex glycyl-l-histidyl-l-lysine-Cu (II) (GHK-Cu) is involved in wound healing and tissue remodeling. Although GHK-Cu exhibits anti-aging and tissue renewing properties, its roles in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) are still unknown. Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo. GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI. Moreover, GHK-Cu attenuated LPS-induced lung histological alterations, suppressed the infiltration of inflammatory cells into the lung parenchyma in LPS-induced ALI in mice. Taken together, these findings demonstrate that GHK-Cu possesses a protective effect in LPS-induced ALI by inhibiting excessive inflammatory responses; accordingly it may represent a novel therapeutic approach for ALI/ARDS.
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