Platelet-rich fibrin elicits an anti-inflammatory response in macrophages in vitro
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 RAW264.7 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 1 beta (IL1 beta) 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 RAW264.7 cells as indicated by the expression of IL1 beta 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.
|Título según WOS:||Platelet-rich fibrin elicits an anti-inflammatory response in macrophages in vitro|
|Título según SCOPUS:||Platelet-rich fibrin elicits an anti-inflammatory response in macrophages in vitro|
|Fecha de publicación:||2020|
|Página de inicio:||244|