Quercetin accelerates full-thickness burn wound repair by modulation of oxidative stress and inflammation

Burn injuries disrupt the skin barrier, incite dysregulated inflammation, oxidative stress, and sepsis, which often delay healing. Quercetin, a bioactive flavonoid, has strong antioxidant and anti-inflammatory effects; however, its specific molecular mechanisms in burn wound healing remain largely unexplored. This study systematically investigated the effects of topical application of quercetin (0.1% and 0.3%, w/v) on full-thickness burn wounds in rats and compared with silver sulfadiazine (1% SSD; reference care). Biochemical and molecular markers related to proliferation, angiogenesis, inflammation, and redox homeostasis were analysed using ELISA, histopathology, immunohistochemistry, and immunoblotting. Topical 0.3% quercetin treatment significantly (p < 0.05) accelerated healing seven days post-wounding by enhancing proliferation (PCNA, TGF-β1), re-epithelialization (cytokeratin 14), angiogenesis (CD31), ECM remodeling (fibronectin), wound contraction (α-SMA), and antioxidant defense (Nrf2, SOD, GST), compared with the control and SSD groups. Quercetin also significantly reduced inflammatory, pain-associated markers (NF-κB, TNF-α, COX-2, substance-P receptor), enhanced calcium homeostasis (TRPV3), and cytoprotection (GRP78). Histopathological observations revealed a reduced epithelial gap, well-organized collagen deposition, and decreased mast cell infiltration after quercetin treatment. These findings provide mechanistic evidence that topical 0.3% quercetin accelerates full-thickness burn wound healing by reducing oxidative stress, inflammation, and pain markers while enhancing endogenous antioxidant defense and promoting tissue regeneration.