PRP as a modulator of inflammation in FLS of RA patients by regulation of galectins and TGF-β1

Abstract

Human FLS cells from RA patients' synovial fluid were cultured in DMEM-F12 medium, characterized by flowcytometry, treated with PRP alone, TNF-α+PRP, SF+PRP, TNF-α alone, and untreated control groups. Expression of Galectin-1, Galectin-3, Galectin-9, and TGF-β1 genes was assessed by Real-Time PCR. In SF+PRP, TNF+PRP, and PRP groups, the gene expression of Galectin-3 was considerably reduced (P>0.05). Galectin-1 and TGF-β1 expression levels were also lowered (P>0.05) in the TNF+PRP groups. Galectin-9 expression increased significantly in the PRP group (P>0.05). Galectin-3 expression was markedly and extensively reduced in multiple study groups after treatment of FLS cells with 10% PRP. Galectin-3 expression was considerably reduced when FLS were exposed to TNF- and synovial fluid in conjunction with PRP to simulate localized body inflammation. Our results showed that PRP may be useful in lowering FLS-induced inflammation in RA patients' joints, particularly when Galectin-3 is involved. In the future, inflammatory illnesses like RA may be treated locally using PRP or its derivatives, which will have a larger immune modulation role and more likely pathways.