Low dose radiation attenuates inflammation and promotes wound healing in a mouse burn model

Burn injuries are devastating traumas that functionally affect a variety of organ systems. As intensive inflammatory responses induced by burns can lead to multiple organ failures and impaired skin regeneration increases risk of infectious complex, multimodal therapeutic approaches are needed.

To investigate the role of low dose radiation (LDR) treatment for regulation of excessive inflammation and wound healing after burn injury.

Mouse burn model was established by generating third-degree burn injury in dorsal skin and local LDR less than 100 mGy was delivered to the mice. After 3 or 12 days after burn injury, systemic inflammation in liver, lung, spleen, and kidney and skin wound healing were assessed. For investigation of molecular mechanisms, HaCaT keratinocytes were administrated with serum from mice with burn injury and alteration of viability and cornification biomarkers are assessed.

In a mouse burn model, expression of proinflammatory cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, were downregulated by LDR in major organs and wound healing capacity was increased by LDR. In skin tissue, we observed the alleviation of reactive oxygen species generation and increased antioxidant gene expression by LDR. In addition, we found that treatment of serum from mice with burn injury and LDR increased proliferation and cornification in HaCaT cells through activation of focal adhesion kinase signaling pathway.

LDR could reduce proinflammatory signaling pathway and increase skin wound healing after burn injury. Therefore, the present study suggested LDR as a novel treatment for burn injury patients.