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Updated: Jan 21, 2026

Characterization of Leukocyte-platelet Rich Fibrin, A Novel Biomaterial
Published on: September 29, 2015
Platelet-rich fibrin elicits an anti-inflammatory response in macrophages in vitro
Jila Nasirzade1,2, Zahra Kargarpour1,2, Sadegh Hasannia2
1Department of Oral Biology, Medical University of Vienna, Vienna, Austria.
Background:
Platelet-rich fibrin (PRF) serves as a reservoir of bioactive molecules to support wound healing and bone regeneration. The beneficial action of PRF might involve macrophage polarization from proinflammatory M1 toward pro-resolving M2 phenotypes. This study aims to evaluate the effect of PRF on macrophage polarization.
Methods:
Murine primary macrophages and RAW 264.7 cells were exposed to saliva and lipopolysaccharides (LPS) with and without PRF lysates obtained by repeated freeze-thawing or the secretome of PRF membranes, termed PRF conditioned medium. The expression of the M1 marker genes interleukin 1β (IL1β) and interleukin 6 (IL6) along with the M2 markers arginase-1 and chitinase-like 3 (Chil3 or YM1) were evaluated by real time polymerase chain reaction. Immunoassay and immunofluorescence staining were performed for IL6 and p65 translocation, a subunit nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), respectively.
Results:
We report here that PRF lysates and PRF conditioned medium, the latter containing the secretome, greatly decreased the proinflammatory response of primary macrophages and RAW 264.7 cells as indicated by the expression of IL1β and IL6. The anti-inflammatory activity of PRF lysates was further confirmed by IL6 immunoassay. Moreover, PRF lysates suppressed the translocation of p65 from the cytoplasm into the nucleus after incubation with saliva. In support of M2 polarization, PRF lysates and PRF conditioned medium enhanced the expression of arginase-1 and YM1 in primary macrophages.
Conclusion:
Our results indicate that PRF holds an anti-inflammatory activity and shifts the macrophage polarization from an M1 toward an M2 phenotype.
Insights
Platelet-rich fibrin (PRF) exhibits anti-inflammatory properties, shifting macrophages from M1 to M2 phenotypes. This finding supports PRF
Area of Science:
- Biomedical Engineering
- Immunology
- Regenerative Medicine
Background:
- Platelet-rich fibrin (PRF) is a source of bioactive molecules crucial for wound healing and bone regeneration.
- PRF's therapeutic effects may stem from its ability to modulate macrophage polarization.
- Macrophages exist in proinflammatory M1 and pro-resolving M2 phenotypes, influencing tissue repair outcomes.
Purpose of the Study:
- To investigate the impact of PRF on macrophage polarization.
- To determine if PRF can shift macrophages from an M1 to an M2 phenotype.
Main Methods:
- Murine primary macrophages and RAW 264.7 cells were treated with PRF lysates or PRF conditioned medium.
- Gene expression of M1 (IL1β, IL6) and M2 (arginase-1, YM1) markers was assessed using real-time PCR.
- IL6 levels and NF-kB p65 translocation were evaluated via immunoassay and immunofluorescence.
Main Results:
- PRF lysates and PRF conditioned medium significantly reduced M1 marker expression (IL1β, IL6) in macrophages.
- PRF demonstrated anti-inflammatory activity, confirmed by decreased IL6 levels and suppressed p65 translocation.
- PRF treatments promoted M2 polarization, evidenced by increased expression of arginase-1 and YM1.
Conclusions:
- PRF possesses significant anti-inflammatory properties.
- PRF effectively induces a shift in macrophage polarization from the M1 to the M2 phenotype.
- These findings highlight PRF's potential in modulating immune responses for therapeutic applications.
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