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.

摘要

总磷脂级分（TPF）具有抗炎特性，并减少了动物模型中的细胞凋亡。我们的目的是在皮肤缺血再灌注（I / R）损伤的小鼠模型中评估TPF对压疮的影响。皮肤I / R损伤是通过在两个磁盘之间夹背皮肤12小时，然后取出磁盘而造成的。在再灌注开始时在I / R区域施用TPF可以显着抑制压力性溃疡的形成。经TPF处理后，伤口区域中性粒细胞和M1巨噬细胞的数量以及促炎介质MCP-1，IL-1β，IL-6和TNF-α的水平降低。经TPF处理的小鼠伤口的胶原蛋白合成和α-SMA阳性微血管密度显着增加。另外，TPF抑制皮肤I / R损伤诱导的凋亡细胞的形成和积累。此外，TPF增加了丝聚蛋白和整合素的表达。总之，TPF可通过调节炎症，胶原蛋白生成，血管生成和皮肤屏障恢复来抑制皮肤I / R损伤诱导的压力性溃疡的形成。因此，外用TPF可能对褥疮等皮肤I / R损伤具有治疗潜力。