Allicin protects against inflammation via suppression of PI3K/AKT/NF-κB signaling pathway in the model of acute cutaneous injury mouse and LPS-induced keratinocyte.

Abstract

BACKGROUND: Wound healing is crucial for tissue repair, with inflammatory regulation being a key determinant of recovery. While Allicin exhibits multifunctional therapeutic properties, its mechanistic basis for anti-inflammatory protection during wound healing requires elucidation. METHODS: In vitro, we established an inflammatory model by stimulating HaCaT cells with lipopolysaccharide (LPS). In vivo, experiments employed a standardized full-thickness excisional wound model (1&#xa0;cm diameter) in mice. Cellular responses were evaluated using CCK-8 assays and scratch tests. Protein expression of inflammatory markers (IL-6, TNF-&#x3b1;), proliferative indicators (PCNA), and PI3K/AKT/NF-&#x3ba;B pathway components (including phosphorylation status) were analyzed through western blotting and immunofluorescence. Pathway specificity was confirmed via PI3K inhibitor (LY294002) pretreatment. Tissue morphology and collagen deposition were assessed using hematoxylin-eosin (H&E) and Masson's trichrome staining. RESULTS: In vitro, Allicin dose-dependently suppressed HaCaT cell within 24&#xa0;h, regardless of LPS stimulation. In vivo, Allicin treatment significantly enhanced wound closure rates (P&#xa0;<&#xa0;0.05) and promoted collagen deposition and re-epithelialization. Significantly reduced protein levels of IL-6, TNF-&#x3b1;, PCNA, PI3K, AKT, and NF-&#x3ba;B (including phosphorylation status) were observed in Allicin group versus LPS-treated group or Injury group (P&#xa0;<&#xa0;0.05) in both Western blotting and immunofluorescence. CONCLUSION: Allicin accelerates wound healing by modulating PI3K/AKT/NF-&#x3ba;B signaling to suppress inflammation and abnormal proliferation.