Therapeutic Mechanism Of Platelet-Rich Plasma On Rheumatoid Arthritis Research

Purpose: Rheumatoid arthritis(RA)is a chronic disease affecting daily life of numerous patients,and uncontrolled proliferation of synovial fibroblasts plays vital roles during the pathology of RA.Platelet-rich plasma(PRP),widely used in tissue regeneration and pain management,is rarely studied in RA.This study aims to investigate the effect of PRP on inflammatory factors and synovial fibroblasts during RA.Methods: We investigated the therapeutic effects and primary mechanism of PRP on a type II collagen-induced arthritis(CIA)mouse model.Inflammatory factors of IL-6,IL-8,IL-17,IL-1?,TNF-? and IFN-? were analyzed in PRP and PBS-treated groups.VEGF,PDGF,IGF-1 and TGF-? expression in peripheral whole blood was also analyzed.Therapeutic efficacy of PRP for RA mice was evaluated by clinical arthritis scores.Rheumatoid fibroblast-like synoviocytes MH7 A cells were stimulated by lipopolysaccharide(LPS)to mimic RA conditions and treated with PRP,after which the concentration of inflammatory factors interleukin(IL)1?,tumor necrosis factor alpha(TNF?)and IL6 in the culture medium was quantified by ELISA.CCK-8 assay,flow cytometry and tube formation assay were performed to assess changes in cell viability,apoptosis and in vitro angiogenesis,respectively.Besides,factors in the phosphoinositide-3-kinase(PI3K)/ v-akt murine thymoma(AKT)signaling were examined.Results: Our preclinical date PRP alleviated the arthritis and reduced humoral andcellular immune responses that led to beneficial effects on histological parameters by joint tissue histological staining.CIA mice treatment with PRP down-regulate expression of IL-6,IL-8,IL-17 A,IL-1?,TNF-?,RANKL and IFN-? in inflammatory tissue.In addition,VEGF,PDGF,IGF-1 and TGF-? expression in peripheral whole blood was increased after treatment with PRP.Furthermore,concentration levels anti-collagen were decreased in the serum on the PRP-treated CIA mice.Results showed that PRP markedly inhibited the production of IL1?,TNF? and IL6(P < 0.05)that was stimulated by LPS.LPS promoted MH7 A cell viability,inhibited apoptosis and accelerated in vitro angiogenesis,while PRP could markedly relieve these effects(P < 0.05).The mRNA and protein levels of AKT1,PI3 K p58 and nuclear factor ?B were elevated by LPS,and then suppressed by PRP(P < 0.01).Conclusions: In conclusion,CIA mice treatment with PRP presented beneficial effects on preventing joint inflammation,cartilage destruction,bone damage and repairing joint tissue.This study uncovers the potential of PRP in inhibiting inflammation,repressing synovial fibroblasts and regulating the PI3K/AKT signaling,providing basic proof for future application of PRP in managing RA.Further investigation is necessary to reveal detailed mechanism of PRP.Purpose: Rheumatoid arthritis(RA)is a chronic disease affecting daily life of numerous patients,and uncontrolled proliferation of synovial fibroblasts plays vital roles during the pathology of RA.Platelet-rich plasma(PRP),widely used in tissue regeneration and pain management,is rarely studied in RA.This study aims to investigate the effect of PRP on inflammatory factor and synovial fibroblasts during RA.Methods: We investigated the therapeutic effects and primary mechanism of PRP on a type II collagen-induced arthritis(CIA)mouse model.Inflammatory factors of IL-6,IL-8,IL-17,IL-1?,TNF-? and IFN-? were analyzed in PRP and PBS-treated groups.VEGF,PDGF,IGF-1 and TGF-? expression in peripheral whole blood was also analyzed.Therapeutic efficacy of PRP for RA mice was evaluated by clinical arthritis scores.Rheumatoid fibroblast-like synoviocytes MH7 A cells were stimulated by lipopolysaccharide(LPS)to mimic RA conditions and treated with PRP,after which the concentration of inflammatory factors interleukin(IL)1?,tumor necrosis factor alpha(TNF?)and IL6 in the culture medium was quantified by ELISA.CCK-8 assay,flow cytometry and tube formation assay were performed to assess changes in cellviability,apoptosis and in vitro angiogenesis,respectively.Besides,factors in the phosphoinositide-3-kinase(PI3K)/ v-akt murine thymoma(AKT)signaling were examined.Results: Our preclinical date PRP alleviated the arthritis and reduced humoral and cellular immune responses that led to beneficial effects on histological parameters by joint tissue histological staining.CIA mice treatment with PRP down-regulate expression of IL-6,IL-8,IL-17 A,IL-1?,TNF-?,RANKL and IFN-? in inflammatory tissue.In addition,VEGF,PDGF,IGF-1 and TGF-? expression in peripheral whole blood was increased after treatment with PRP.Furthermore,concentration levels anti-collagen were decreased in the serum on the PRP-treated CIA mice.Results showed that PRP markedly inhibited the production of IL1?,TNF? and IL6(P < 0.05)that was stimulated by LPS.LPS promoted MH7 A cell viability,inhibited apoptosis and accelerated in vitro angiogenesis,while PRP could markedly relieve these effects(P < 0.05).The m RNA and protein levels of AKT1,PI3 K p58 and nuclear factor ?B were elevated by LPS,and then suppressed by PRP(P < 0.01).Conclusions: In conclusion,CIA mice treatment with PRP presented beneficial effects on preventing joint inflammation,cartilage destruction,bone damage and repairing joint tissue.This study uncovers the potential of PRP in inhibiting inflammation,repressing synovial fibroblasts and regulating the PI3K/AKT signaling,providing basic proof for future application of PRP in managing RA.Further investigation is necessary to reveal detailed mechanism of PRP.