Dihydromyricetin/F127 enhances fibroblast and endothelial responses and accelerates healing in debrided deep partial thickness burn wounds.

Abstract

Debrided burn wounds require coordinated fibroblast, endothelial, and inflammatory responses for effective tissue repair. Dihydromyricetin (DHM) exhibits antioxidant and anti-inflammatory activities, but its concentration-response profile remains unclear. This study evaluated DHM in L929 fibroblasts and HUVECs and assessed a topical DHM/F127 formulation in a debrided contact-burn wound model. In vitro, 25-50 μM DHM increased L929 CCK-8 metabolic activity and scratch closure, while concurrent DHM treatment attenuated H₂O₂ associated oxidative stress. In HUVECs, 50 μM DHM increased scratch closure, and 25-50 μM enhanced tube formation. For in vivo validation, a standardized deep partial-thickness contact burn model was established in BALB/c mice, followed by debridement at 24 h after injury. Ten mice per group were randomly assigned to day 7 and day 14 endpoint cohorts, with five mice per endpoint. Wounds were treated daily with F127 or DHM/F127 containing 0.5 mg/mL DHM. Compared with F127, DHM/F127 further accelerated wound closure and reduced inflammatory infiltration at both endpoints, decreased MPO expression on day 7, and increased CD34 expression on day 14. These findings characterize DHM-associated fibroblast and endothelial responses and demonstrate additional tissue-level repair effects of DHM/F127 relative to F127 in debrided burn wounds.