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Updated: Oct 13, 2025

Characterization of Leukocyte-platelet Rich Fibrin, A Novel Biomaterial
Published on: September 29, 2015
Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells
Zahra Kargarpour1, Jila Nasirzade1, Layla Panahipour1
1Department of Oral Biology, Medical University of Vienna, 1090 Vienna, Austria.
Abstract:
Chronic inflammation is a pathological process where cells of the mesenchymal lineage become a major source of inflammatory mediators. Platelet-rich fibrin (PRF) has been shown to possess potent anti-inflammatory activity in macrophages, but its impact on mesenchymal cells has not been investigated. The aim of this study was, therefore, to expose mesenchymal cells to inflammatory cytokines together with lysates generated from liquid platelet-poor plasma (PPP), the cell-rich buffy coat layer (BC; concentrated-PRF or C-PRF), and the remaining red clot layer (RC), following centrifugation of blood. Heating PPP generates an albumin gel (Alb-gel) that when mixed back with C-PRF produces Alb-PRF. Membranes prepared from solid PRF were also subjected to lysis. We report here that lysates of PPP, BC, and PRF decreased the cytokine-induced expression of interleukin 6 (IL6) and nitric oxide synthase (iNOS) in the bone marrow-derived ST2 cells. Consistently, PPP, BC, and PRF greatly decreased the phosphorylation and nuclear translocation of p65 in ST2 cells. The inflammatory response caused by Pam3CSK4 was reduced accordingly. Moreover, PPP, BC, and PRF reduced the enhanced expression of inflammatory mediators IL6 and iNOS in 3T3-L1 pre-adipocyte mesenchymal cells, and iNOS and CCL5 in murine calvarial cells. Surprisingly, PRF lysates were not effective in reducing the inflammatory response of human gingival fibroblasts and HSC2 epithelial cells. The data from the present study suggest that both liquid PRF and solid PRF exert potent anti-inflammatory activity in murine mesenchymal cells.
Insights
Platelet-rich fibrin (PRF) and its components effectively reduce inflammatory responses in various murine mesenchymal cells. This study demonstrates PRF
Area of Science:
- Regenerative Medicine
- Immunology
- Cell Biology
Background:
- Chronic inflammation involves mesenchymal cells producing inflammatory mediators.
- Platelet-rich fibrin (PRF) shows anti-inflammatory effects in macrophages, but its impact on mesenchymal cells is unknown.
Purpose of the Study:
- To investigate the anti-inflammatory effects of platelet-rich fibrin (PRF) and its blood-derived components on mesenchymal cells.
Main Methods:
- Mesenchymal cells (ST2, 3T3-L1, murine calvarial cells) were exposed to inflammatory cytokines and lysates from platelet-poor plasma (PPP), buffy coat (BC), and PRF.
- Western blotting and nuclear translocation assays assessed inflammatory signaling pathways (p65 phosphorylation).
- Expression of inflammatory mediators (IL6, iNOS, CCL5) was quantified.
Main Results:
- Lysates of PPP, BC, and PRF significantly reduced cytokine-induced IL6 and iNOS expression in ST2 cells.
- These components also decreased p65 phosphorylation and nuclear translocation in ST2 cells.
- PPP, BC, and PRF diminished inflammatory mediators in 3T3-L1 and murine calvarial cells, but not in human gingival fibroblasts or HSC2 cells.
Conclusions:
- Both liquid and solid forms of PRF exhibit potent anti-inflammatory activity in murine mesenchymal cells.
- The anti-inflammatory effects are mediated through the suppression of key inflammatory signaling pathways.
- PRF components may hold therapeutic potential for inflammatory conditions involving mesenchymal cells.
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