Highlights
• CGE significantly accelerated the healing rate of diabetic ulcer wounds, facilitated re-epithelialization, and downregulated the transcription levels of inflammatory cytokines interleukin (IL)-1β and tumor necrosis factor-α (TNF-α)
• CGE could reduce the abundance of pathogenic bacteria such as Staphylococcus aureus and significantly enrich Escherichia coli (E. coli) by regulating the microecology of diabetic ulcer bacteria
• E. coli can increase the secretion level of L-glutamate under CGE treatment, which promotes the cell proliferation and migration level of keratinocytes and fibroblasts as well as epithelialization and tissue barrier regeneration
• Modulation of commensal wound microbiome may be a new therapeutic strategy for the treatment of diabetic wound repair

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