Study summary · research use only
Protective effects of GHK-Cu in bleomycin-induced pulmonary fibrosis via anti-oxidative stress and anti-inflammation pathways
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this mouse (C57BL/6j) study, bleomycin (3 mg/kg) was administered via tracheal instillation to induce pulmonary fibrosis, and GHK-Cu (glycyl-L-histidyl-L-lysine copper complex) was injected intraperitoneally at 0.2, 2, or 20 μg/g/day in 0.5 ml PBS on alternate days, with tissue evaluated 21 days after the bleomycin challenge. The abstract reports that GHK-Cu was associated with reduced inflammatory and fibrotic pathological changes, lower levels of inflammatory cytokines TNF-α and IL-6 and MPO activity in bronchoalveolar lavage fluid, and reduced collagen deposition. GHK-Cu treatment was also associated with reversal of the MMP-9/TIMP-1 imbalance and partial prevention of epithelial-mesenchymal transition via Nrf2, NF-κB, and TGFβ1/Smad2/3 signaling, including Smad2/3 phosphorylation.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a serious lung problem with advancing and diffusive pulmonary fibrosis as the pathologic basis, and with oxidative stress and inflammation as the key pathogenesis. Glycyl-L-histidyl-l-lysine (GHK) is a tripeptide participating into wound healing and regeneration. GHK-Cu complexes improve GHK bioavailability. Thus, the current study aimed to explore the therapeutic role of GHK-Cu on bleomycin (BLM)-induced pulmonary fibrosis in a mouse model. BLM (3 mg/kg) was administered via tracheal instillation (TI) to induce a pulmonary fibrosis model in C57BL/6j mice 21 days after the challenge of BLM. GHK-Cu was injected intraperitoneally (i.p.) at different dosage of 0.2, 2 and 20 μg/g/day in 0.5 ml PBS on alternate day. The histological changes, inflammation response, the collagen deposition and epithelial-mesenchymal transition (EMT) was evaluated in the lung tissue. EMT was evaluated by ɑ-SMA and fibronectin expression in the lung tissue. NF-κB p65, Nrf2 and TGFβ1/Smad2/3 signalling pathways were detected by immunoblotting analysis. GHK-Cu complex inhibited BLM-induced inflammatory and fibrotic pathological changes, alleviated the inflammatory response in the BALF by reducing the levels of the inflammatory cytokines, TNF-ɑ and IL-6 and the activity of MPO as well as reduced collagen deposition. In addition, the GHK-Cu treatment significantly reversed the MMP-9/TIMP-1 imbalance and partially prevented EMT via Nrf2, NF-κB and TGFβ1 pathways, as well as Smad2/3 phosphorylation. GHK-Cu presented a protective effect in BLM-induced inflammation and oxidative stress by inhibiting EMT progression and suppressing TGFβ1/Smad2/3 signalling in pulmonary fibrosis.
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