2. Academic Validation
  3. Baicalin attenuates burn wound progression by suppressing PANoptosis in the zone of stasis

Baicalin attenuates burn wound progression by suppressing PANoptosis in the zone of stasis

  • Surgery. 2026 Jun:194:110148. doi: 10.1016/j.surg.2026.110148.
Mengjing Xiao 1,  Peirong Zhang 2,  Xiaofang Zou 3,  Hongming Yang 4
Affiliations

Affiliations

  • 1 Department of Burn Plastic and Aesthetic Surgery, South China Hospital, Medical School, Shenzhen University, Shenzhen, P.R. China. Electronic address: [email protected].
  • 2 Inpatient Ward 1, Songhe Care Hospital, Guangzhou, P.R. China.
  • 3 Department of Burn and Plastic Surgery, Air Force Characteristic Medical Center, Beijing, China.
  • 4 Department of Burn Plastic and Aesthetic Surgery, South China Hospital, Medical School, Shenzhen University, Shenzhen, P.R. China.
PMID: 41844447 DOI: 10.1016/j.surg.2026.110148
Abstract

Background: The early progression of burn wounds poses a significant clinical challenge. Although inflammatory cell death is thought to be involved, the role of the newly discovered integrated cell death pathway PANoptosis in burn injuries has not yet been studied. Baicalin is a natural compound with anti-inflammatory properties and has therapeutic potential, but its impact on burn progression and PANoptosis is unknown.

Methods: A rat comb burn model was established. PANoptosis activation was assessed in the zone of stasis via Western blot, immunohistochemistry, and immunofluorescence for key markers (ZBP1, pMLKL, cleaved GSDMD, cleaved Caspase-3, and ASC). In the intervention study, baicalin (100 mg/kg) or vehicle was administered for 7 days. PANoptosis markers, inflammatory cytokines (interleukin 1β, interleukin 6, interleukin 18, tumor necrosis factor α), myeloperoxidase activity, and histopathologic wound progression were evaluated.

Results: Burn injury induced time-dependent PANoptosis activation, characterized by coordinated upregulation of ZBP1, pMLKL, cleaved GSDMD, and cleaved Caspase-3. Immunofluorescence confirmed PANoptosome assembly via ASC/cleaved Caspase-3 colocalization. Baicalin treatment significantly suppressed all 3 PANoptosis executers, disrupted complex formation, reduced proinflammatory cytokines, and myeloperoxidase activity. Importantly, baicalin treatment significantly reduced the progression of burn wounds at day 7, as evidenced by diminished tissue necrosis and improved tissue architecture.

Conclusion: Our study identifies PANoptosis as a novel pathogenic mechanism contributing to burn wound progression. We further demonstrate that baicalin is an effective therapeutic agent that alleviates tissue damage possibly by inhibiting the PANoptosis pathway and its associated inflammatory cascade. These findings provide a new mechanistic understanding and highlight the therapeutic potential of baicalin for preventing burn wound deepening.

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