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ABSTRACT
The total phospholipid fraction (TPF) has anti-inflammatory properties and reduces apoptosis in animal models. Our objective was to assess the effects of TPF on pressure ulcers in a mouse model of cutaneous ischemic-reperfusion (I/R) injury. Cutaneous I/R injury was created by trapping the dorsal skin between two magnetic disks for 12 h, followed by disk removal. TPF administration in I/R areas at the beginning of reperfusion significantly inhibited the formation of pressure ulcers. The number of neutrophils and M1 macrophages and the levels of proinflammatory mediators MCP-1, IL-1β, IL-6, and TNF-α in the wound area were reduced upon TPF treatment. Collagen synthesis and α-SMA-positive microvessel density significantly increased in the wounds of TPF-treated mice. Additionally, TPF inhibited cutaneous I/R injury-induced formation and accumulation of apoptotic cells. Moreover, TPF increased the expression of filaggrin and involucrin. In conclusion, TPF may inhibit cutaneous I/R injury-induced formation of pressure ulcers by regulating inflammation, collagen production, angiogenesis, and skin barrier restoration. Therefore, exogenous application of TPF might have therapeutic potential with respect to cutaneous I/R injuries like decubitus ulcers.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
Due to the nature of this research, participants of this study did not agree for their data to be shared publicly, so supporting data is not available.