Department of Plastic and Reconstructive Surgery, Yonsei University, College of Medicine, Seoul, Republic of Korea.
Department of Plastic and Reconstructive Surgery, Gachon University Gil Medical Center, Incheon, Republic of Korea.
Int J Med Sci. 2017 Jul 19;14(9):829-839. doi: 10.7150/ijms.19573. eCollection 2017.
Ischemia-reperfusion (I/R) injury is a leading cause of surgical skin flap compromise and organ dysfunction. Platelet-rich plasma (PRP) is an abundant reserve of various growth factors. Activated platelets play a role in endothelial damage during I/R injury; however, exogenous PRP could inhibit the production of reactive oxygen species. The goal of this study was to investigate the effect of PRP on I/R injury. Four groups (n=30) of C57BL/6N mice with lateral thoracic artery island flaps were used. Group A, the control group, received flap elevation and repositioning. Group B received PRP and repositioning. Group C had 4 hours of ischemia and then were reperfused. Group D received PRP, had 4 hours of ischemia, and then were reperfused. The survival area of flap tissue and blood perfusion were assessed. Histological evaluation included neutrophil counts. Reactive oxygen species and proinflammatory cytokines were measured to evaluate I/R injury. Protein expression of phosphorylated apoptosis signaling regulating kinase-1 (pASK-1), p38MAPK, and pNF-κB was measured by western blot. PRP treatment enhanced the survival area and perfusion of the flap, reduced neutrophil accumulation in mice subjected to I/R injury. PRP treatment also showed a protective effect, with decreases in nitric oxide, myeloperoxidase, malondialdehyde concentrations. Additionally, PRP suppresses monocyte chemotactic protein-1, TNF-α, IL-1β, and IL-6. Finally, PRP decreased ASK-1 and NF-κB expression in tissues with I/R injury. PRP acts as a protective factor during flap I/R injury by reducing reactive oxygen species level and proinflammatory cytokines via decreased expression of pASK-1 and pNF-κB.
缺血再灌注（I/R）损伤是手术皮瓣失偿和器官功能障碍的主要原因。富含血小板的血浆（PRP）是各种生长因子的丰富储备。活化的血小板在 I/R 损伤期间在血管内皮损伤中起作用；然而，外源性 PRP 可以抑制活性氧的产生。本研究旨在探讨 PRP 对 I/R 损伤的影响。使用 C57BL/6N 小鼠的侧胸动脉岛皮瓣的四组（n=30）。A 组为对照组，接受皮瓣抬高和复位。B 组接受 PRP 和复位。C 组缺血 4 小时，然后再灌注。D 组接受 PRP，缺血 4 小时，然后再灌注。评估皮瓣组织的存活面积和血液灌注。组织学评估包括中性粒细胞计数。通过测量活性氧和促炎细胞因子来评估 I/R 损伤。通过 Western blot 测量磷酸化凋亡信号调节激酶-1（pASK-1）、p38MAPK 和 pNF-κB 的蛋白表达。PRP 治疗可增强 I/R 损伤小鼠皮瓣的存活面积和灌注，减少中性粒细胞聚集。PRP 治疗还表现出保护作用，降低了一氧化氮、髓过氧化物酶和丙二醛的浓度。此外，PRP 抑制单核细胞趋化蛋白-1、TNF-α、IL-1β 和 IL-6。最后，PRP 降低了 I/R 损伤组织中 ASK-1 和 NF-κB 的表达。PRP 通过降低活性氧水平和促炎细胞因子来减少 pASK-1 和 pNF-κB 的表达，从而在皮瓣 I/R 损伤中充当保护因子。
