Epigallocatechin Gallate Prevents Burn Wound Progression Through Inhibiting Mitochondrial DNA-Induced Inflammation

This study aims to investigate the effect of epigallocatechin gallate on experimental burn wound progression. A deep second-degree burn was produced on male Wistar rats. Epigallocatechin gallate was systemically administrated as treatment intervention. The mitochondrial DNA level in serum and the level of proinflammatory cytokines in burn wounds were detected. The malonaldehyde content, the myeloperoxidase activity, and the nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 inflammasome level in the burn wounds were measured. The histopathological examination of burn wounds was performed, and the time to wound reepithelialization was recorded. Burn resulted in remarkably higher level of mitochondrial DNA release in serum and proinflammatory cytokines in burn wounds. Moreover, the malonaldehyde content, myeloperoxidase activity, and nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 inflammasome level in burn wounds were significantly higher than that of sham burn. Epigallocatechin gallate treatment significantly reduced mitochondrial DNA level in serum and inflammatory response in burn wounds. Furthermore, the burn wound depth of rats in epigallocatechin gallate group was markedly attenuated, and the wound reepithelialization time was accelerated. Epigallocatechin gallate ameliorated burn wound progression probably through inhibiting the mitochondrial DNA-induced inflammation and protecting wounds from inflammatory infiltration and oxidative damage.