Phospholipid fraction has protective effect by improving inflammation and skin barrier function in ischemia-reperfusion injury in mice
- Authors
- Kim, S.-Y.; Kim, Y.-J.; Lee, E.; Choi, S.H.; Moon, J.S.; An, H.S.; Ji, E.S.; Na, J.; Kim, B.J.
- Issue Date
- 2020
- Publisher
- Taylor and Francis Ltd.
- Keywords
- collagen; inflammation; macrophages; microvessel; Phospholipid; pressure ulcer
- Citation
- All Life, v.13, no.1, pp 623 - 633
- Pages
- 11
- Journal Title
- All Life
- Volume
- 13
- Number
- 1
- Start Page
- 623
- End Page
- 633
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/52514
- DOI
- 10.1080/26895293.2020.1838334
- ISSN
- 2689-5293
2689-5307
- 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. © 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
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