Mitochondrial DNA-induced Inflammation Response of Epigallocatechin Gallate for Burn Wound

Background: Burns are dynamic wounds that may present a progressive deepening and expansion of the initial burn area, a process defined as burn wound progression. There are multiple factors involved in the pathophysiology of burn wound progression, however, the exact mechanisms are unclear and the therapeutic modalities are limited. This study is aimed to investigate the effect of epigallocatechin gallate on experimental burn wound progression.

Methods: A deep second-degree burn was produced on male Wistar rats. Epigallocatechin gallate was systemically administrated as a treatment intervention. Mitochondrial DNA level in serum and level of proinflammatory cytokines in burn wounds was detected. Malonaldehyde content, myeloperoxidase activity, and the nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3 inflammasome levels in the burn wounds were measured. The histopathological examination of burn wounds was performed and the time to wound re-epithelialization was recorded.

Results: Burn resulted in remarkably higher levels 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 levels in serum and inflammatory response in burn wounds. Furthermore, the burn wound depth of rats in the epigallocatechin gallate group was markedly attenuated and the wound re-epithelialization time was accelerated.

Conclusion: Epigallocatechin gallate ameliorated burn wound progression probably by inhibiting mitochondrial DNA-induced inflammation and protecting wounds from inflammatory infiltration and oxidative damage.