Platelet‐Rich Fibrin Promotes Wound Healing by Regulating miR‐155 Levels in Diabetic Foot Ulcer

伤口愈合 医学 糖尿病足 糖尿病足溃疡 纤维蛋白 富血小板纤维蛋白 内科学 缺氧(环境) 糖尿病 泌尿科 外科 内分泌学 免疫学 化学 有机化学 氧气
作者
Jiajia Zhang,Dongxin Chen,Di Tang,Xianmei Wen,Ling Yue,Guangda Xiang,Tao Li
出处
期刊:Wound Repair and Regeneration [Wiley]
卷期号:33 (4): e70073-e70073 被引量:1
标识
DOI:10.1111/wrr.70073
摘要

Diabetic foot ulcer (DFU) is a kind of refractory wound, with elevated miR-155 impeding the healing process. Platelet-rich fibrin (PRF) enhances tissue regeneration after injury, yet its therapeutic role and mechanisms in DFU remain unclear. The miR-155 levels in wound margin tissues from 20 DFU and 20 non-diabetic patients were compared. Sixty DFU patients meeting the inclusion criteria were divided into the control group (n = 36) and the PRF group (n = 24) after receiving basic treatment. Baseline clinical characteristics and healing progress were analysed between groups. The correlation between miR-155 levels in wound margin tissues and baseline clinical data were analysed, and the independent influencing factors of wound healing were explored by COX regression analysis. The effect of PRF on the miR-155, hypoxia inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF), and vascular density in the wound margin tissue was measured. Elevated miR-155 expression was observed in DFU compared to non-diabetic wounds. The miR-155 levels were positively associated with Wagner grading (R = 0.578). Accelerated wound healing was demonstrated in the PRF group versus controls via Kaplan-Meier analysis. Multivariate Cox regression found that miR-155 (HR = 0.87, 95% CI: 0.79-0.97) and PRF intervention (HR = 3.21, 95% CI: 1.70-6.06) were statistically significant for wound healing time. After 15-day PRF interventions, miR-155 levels were suppressed, while HIF-1α and VEGF expression and vascular density were increased in PRF-treated wound margin tissues. PRF promotes the DFU healing via decreasing miR-155 levels in the wound margin tissue, enhancing the expression of HIF-1α and VEGF, and accelerating angiogenesis. These findings provide new evidence from evidence-based medicine and mechanistic insights for the application of PRF in treating DFU.
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