Maxillofacial Surgery Department, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Aesthet Surg J. 2020 Aug 14;40(9):NP530-NP545. doi: 10.1093/asj/sjaa084.
Platelet-rich fibrin (PRF) can promote fat graft survival, but limited data are currently available, and the underlying mechanism of this effect has not yet been explained.
The aim of this study was to explore the mechanism by which PRF promotes fat graft survival, from the aspects of angiogenesis, adipogenesis, cellular apoptosis, and collagen production.
Nude mice were randomly assigned to a PRF group (subcutaneously injected with PRF and fat in the ratio of 1:5 by volume) and a control group (subcutaneously injected with normal saline and fat in the ratio of 1:5 by volume). On days 0, 3, 7, 14, 21, and 28 after transplantation, graft samples (n = 12) were obtained for quantification of target growth factors. In weeks 1, 2, 3, and 4 after transplantation, graft samples (n = 12) were obtained for the following evaluations. The volume and weight retention rates were calculated; gene and protein expression of vascular endothelial growth factor A (VEGF-A), peroxisome proliferator-activated receptor γ (PPAR-γ), COL1-A1, and BAX were evaluated; hematoxylin & eosin staining, Masson's trichrome staining, α smooth muscle actin staining, and perilipin-1 staining were performed to evaluate graft survival.
After transplantation, the concentrations of growth factors produced by the fat increased to varying degrees, and the addition of PRF made these concentration changes ever greater. Compared with the control group, the PRF group had a higher volume and weight retention rate, a higher expression level of VEGF-A and PPAR-γ, a lower expression level of COL1-A1 and BAX, a higher vessel density, less fibrosis, and more viable adipocytes.
PRF can promote autocrine function of the grafted fat to produce more growth factors. It greatly increased fat retention rate, possibly by promoting vascularization and adipogenic differentiation, inhibiting cellular apoptosis, and regulating collagen production.
富血小板纤维蛋白（PRF）可促进脂肪移植物存活，但目前数据有限，其作用机制尚未阐明。
本研究旨在从血管生成、脂肪生成、细胞凋亡和胶原产生等方面探讨 PRF 促进脂肪移植物存活的机制。
将裸鼠随机分为 PRF 组（以 1:5 的体积比皮下注射 PRF 和脂肪）和对照组（以 1:5 的体积比皮下注射生理盐水和脂肪）。在移植后 0、3、7、14、21 和 28 天，获取移植物样本（n=12）以定量检测目标生长因子。在移植后 1、2、3 和 4 周，获取移植物样本（n=12）进行以下评估。计算体积和重量保留率；评估血管内皮生长因子 A（VEGF-A）、过氧化物酶体增殖物激活受体γ（PPAR-γ）、COL1-A1 和 BAX 的基因和蛋白表达；进行苏木精和伊红染色、马松三色染色、α平滑肌肌动蛋白染色和 perilipin-1 染色以评估移植物存活。
移植后，脂肪产生的生长因子浓度不同程度增加，添加 PRF 使这些浓度变化更大。与对照组相比，PRF 组的体积和重量保留率更高，VEGF-A 和 PPAR-γ 的表达水平更高，COL1-A1 和 BAX 的表达水平更低，血管密度更高，纤维化程度更低，存活的脂肪细胞更多。
PRF 可促进移植脂肪的自分泌功能产生更多的生长因子。它大大提高了脂肪保留率，可能通过促进血管生成和脂肪生成分化、抑制细胞凋亡和调节胶原产生来实现。
