Anti‐inflammation Ameliorates Repairment of Frostbite‐induced Skin Injuries

Frostbite occurs when tissues freeze with cold external temperature. Freeze (ice crystals) destructs the cells and blood vessels, increases permeability in vessel walls and blood leaks into the tissues, and causes inflammation‐related further tissue damage. A mouse model of skin frostbite injuries was used to observe the effect of dexamethasone (Dex) on morphological recovery of damaged skin. Under anesthetized condition, C57/BL6 mice were subjected to 5 minutes of the freezing by placing magnets pre‐frozen in dry ice (−20°C) to create frostbite injuries on back skin within 3‐cm diameter circle. Dex treatment (1 mg/kg/day, i.p.) began on the day of frostbite induction and lasted for 7 days. Histological data demonstrated that frostbite resulted in swelling and severe skin damage from the first day, including epidermal necrosis and loss, blood vessel breaking, liquid leakage, degeneration of the panniculus adiposus and carnosus. Pro‐inflammatory factors (IL‐1β and TNFα) were elevated from day 3 to day 14 after frostbite (p < 0.05, compared to control), reaching the maximum level at day 7 after frostbite. After 7 days of frostbite, the skin tissue starts to regenerate. Treatment with Dex attenuated the elevation of TNFα and IL‐1β (p<0.05, compared to frostbite group), promoted CD31 expression (a marker for vascularization; p<0.05, compared to frostbite group), and accelerated collagen deposition and wound closure. These results suggest that Dex treatment attenuates frostbite‐induced inflammation and improves the tissue repairment.