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<p>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 (<i>p</i> &lt; 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月22日

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  • Divya Yadav,
  • Ananya Mahajan,
  • Alpesh K. Sharma,
  • Ashok Priyadarshi,
  • Asheesh Gupta

摘要

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.