Platelet-rich plasma inhibits inflammatory factors and represses rheumatoid fibroblast-like synoviocytes in rheumatoid arthritis

Original Article

DOI: 10.1007/s10238-017-0449-2

Cite this article as:
Tong, S., Liu, J. & Zhang, C. Clin Exp Med (2017). doi:10.1007/s10238-017-0449-2


Rheumatoid arthritis (RA) is a chronic disease affecting daily life of numerous patients, and uncontrolled proliferation of synovial fibroblasts plays vital role 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 synovial fibroblasts during RA. Rheumatoid fibroblast-like synoviocyte MH7A cells were stimulated by lipopolysaccharide (LPS) to simulate RA conditions and treated with PRP, after that the concentration of inflammatory factors interleukin (IL) 1β, tumor necrosis factor alpha (TNFα) and IL6 in the supernatant of culture medium was quantified by ELISA. MTT assay, flow cytometry and tube formation assay were performed to assess changes in cell viability, apoptosis and effect on angiogenesis in vitro, respectively. Besides, the expression levels of main factors in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signal pathway were examined. Results showed that PRP markedly inhibited the production of IL1β, TNFα and IL6 (P < 0.05) that was stimulated by LPS. LPS promoted MH7A cell viability, inhibited apoptosis and accelerated angiogenesis in vitro, while PRP could markedly relieve these effects (P < 0.05). The mRNA and protein levels of AKT1, PI3K (p58) and nuclear factor κ beta were elevated by LPS and then suppressed by PRP (P < 0.01). This study uncovered 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.


Rheumatoid arthritis Platelet-rich plasma Inflammatory factor Angiogenesis Phosphoinositide 3-kinase 

Copyright information

© Springer International Publishing Switzerland 2017

Authors and Affiliations

  1. 1.Department of Orthopaedics, Shanghai Sixth People’s HospitalShanghai Jiaotong UniversityShanghaiChina
  2. 2.Department of Orthopaedics, Shanghai Ruijin HospitalShanghai Jiaotong University School of MedicineShanghaiChina

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