Pretreatment with platelet-rich plasma protects against ischemia-reperfusion induced flap injury by deactivating the JAK/STAT pathway in mice

• Published in: Molecular medicine (Cambridge, Mass.) Vol. 30; no. 1; p. 18
• Main Authors: Su, Linlin, Xie, Songtao, Li, Ting, Jia, Yanhui, Wang, Yunchuan
• Format: Journal Article
• Language: English
• Published: England BMC 01.02.2024
• Subjects: Apoptosis; Inflammatory response; Ischemia–reperfusion; Oxidative stress; Platelet-rich plasma; Oxidative stress; Inflammatory response; Ischemia–reperfusion; Platelet-rich plasma; Apoptosis
• ISSN: 1528-3658; 1528-3658
• DOI: 10.1186/s10020-024-00781-3

Ischemia-reperfusion (I/R) injury is a major cause of surgical skin flap compromise and organ dysfunction. Platelet-rich plasma (PRP) is an autologous product rich in growth factors, with tissue regenerative potential. PRP has shown promise in multiple I/R-induced tissue injuries, but its effects on skin flap injury remain unexplored. We evaluated the effects of PRP on I/R-injured skin flaps, optimal timing of PRP administration, and the involved mechanisms. PRP protected against I/R-induced skin flap injury by improving flap survival, promoting blood perfusion and angiogenesis, suppressing oxidative stress and inflammatory response, and reducing apoptosis, at least partly via deactivating Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signalling pathway. PRP given before ischemia displayed overall advantages over that given before reperfusion or during reperfusion. In addition, PRP pretreatment had a stronger ability to reverse I/R-induced JAK/STAT activation and apoptosis than AG490, a specific inhibitor of JAK/STAT signalling. This study firstly demonstrates the protective role of PRP against I/R-injured skin flaps through negative regulation of JAK/STAT activation, with PRP pretreatment showing optimal therapeutic effects.