Graphene–peptide nanofibers as potential diabetic wound dressings: An in vitro study

Diabetic foot ulcers (DFUs) represent a major complication of diabetes mellitus and are frequently associated with previously unrecognized diabetic neuropathy, chronic microbial colonization, and biofilm-mediated infections that markedly impair wound healing. To address these unmet clinical needs, we prepared a graphene-based nanofiber formulation combined with a computationally engineered antimicrobial peptide (Peptide A). The antimicrobial performance of Peptide A, graphene nanofibers, and the combined Peptide A@Graphene formulation was evaluated using OD-based growth assays against clinically relevant bacterial and fungal pathogens commonly detected in DFUs. Short-term in vitro cytotoxicity of the Peptide A@Graphene formulation was assessed in human keratinocytes and dermal fibroblasts using LDH release, while AlamarBlue was used to assess metabolic activity. Genotoxicity assessment using the comet assay was performed only for Peptide A and not for the complete Peptide A@Graphene formulation. Basal CXCL-8/IL-8 secretion was also quantified in culture supernatants to assess cytokine modulation under non-induced in vitro conditions. Peptide A@Graphene nanofibers showed broad OD-based antimicrobial and antifungal growth-signal reductions and reduced basal CXCL-8/IL-8 secretion in vitro. No detectable short-term cytotoxic effects were observed for the Peptide A@Graphene formulation under the tested conditions, while Peptide A alone did not induce detectable DNA damage in fibroblasts. However, because genotoxicity was not assessed for the complete Peptide A@Graphene formulation, further studies are required to establish the long-term and formulation-level safety profile. Overall, these findings support Peptide A@Graphene nanofibers as a promising multifunctional in vitro wound-care candidate that combines OD-based antimicrobial growth-signal reductions, maintenance of cellular metabolic activity, absence of detectable short-term LDH release, and modulation of basal CXCL-8/IL-8 secretion relevant to DFU management.