Ameliorative Effect of a Chenopodium formosanum-Derived Peptide on Diabetic Wound Healing and Fibroblast Dysfunction

Oxidative stress contributes to fibroblast dysfunction in diabetic wounds. We evaluated a previously characterized glycine-rich peptide derived from Rhizopus oligosporus-fermented germinated Chenopodium formosanum (FGP) in male diabetic db/db mice and NIH3T3 fibroblasts. Topical FGP (20 or 100 ppm) was assessed by wound-area measurements and histology over 14 days, whereas fibroblasts exposed to 100 mM glucose were evaluated for viability, gap closure, intracellular reactive oxygen species (ROS), type I collagen expression, and repair-associated proteins. On day 14, wound contraction reached 77.6% with 100 ppm FGP and was greater than in untreated wounds (p < 0.05). In fibroblasts, 50 and 100 ppm FGP reduced ROS by approximately 37% and 79%, increased type I collagen expression by approximately 80–90%, and reduced the p-p65 NF-κB/p65 NF-κB ratio by 38% and 48% and the MMP-9/TIMP-1 ratio by 61% and 66%, respectively (p < 0.05). Both concentrations also improved gap closure, whereas VEGF expression increased significantly only at 50 ppm. Among the concentrations tested, 100 ppm showed the most consistent overall activity and is proposed as the preferred concentration for further preclinical evaluation, although formal dose optimization remains necessary. These findings support further investigation of FGP for diabetic wound repair, while tissue-level mechanisms and long-term outcomes remain to be established.