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s / Osteoarthritis and Cartilage 28 (2020) S86eS527 S120 EVs from the two autologous blood derived products PRP and the cell free alternative hyperacute (hypACT) serum in an inflammation model was investigated. Methods: PRP and hypACT serum were generated by double or single centrifugation of whole blood. EVs were isolated from PRP and hypACT serum by differential ultracentrifugation and concentration and size of the EVs were determined by Nanoparticle Tracking Analysis (NTA). To generate an inflammation model, human primary monocytes were differentiated and activated into inflammatory (M1) macrophages and patient-derived OA chondrocytes were co-cultivated together with these M1 macrophages to mimic an inflammatory environment as present in OA. Culture medium was supplemented with EVs isolated from either PRP or hypACT serum and as control medium was supplemented with either FCS or EV-depleted FCS. Secretion of the inflammatory cytokines IL6, TNFa and IL1b were meassured by ELISA. mRNA expression of the cartilage specific genes SOX9, Collagen 2 and Aggrecan as well as of the matrix degrading enzymes MMP3 and MMP13 was assessed by RT-PCR. Protein expression of NFkb and COX2, proteins known to be involved in cartilage degradation during OA, was determined by Western Blot. Results: In the presence of EVsisolated from blood derived products, secretion of inflammatory cytokines was strongly reduced within the inflammationmodel. In addition, expression of chondrogenic genes was upregulated when EVs were added to the medium. Furthermore, EVs could reduce the expression of the transcription factor NFkb and hence also of its target gene COX2. Conclusions: Within an inflammation model, EVs from blood derived products harbor the potential to downregulate the secretion of inflammatory cytokines as well as the expression of proteins promoting extracellular matrix degradation. On the other hand, EVs can revert the osteoarthritic phenotype of patient-derived OA chondrocytes to a more hyaline one. Taken together, EVs from blood derived products can overcome the limits of using the whole blood derived product for cartilage regeneration while offering comparable biological effects. They can be seen as a minimally invasive injective biological approach for the treatment of OA. 165 BOSWELLIA SERRATA EXTRACT AND CURCUMIN INCREASE GDF15 PRODUCTION BY HUMAN PRIMARY OSTEOARTHRITIS CHONDROCYTES: A NEW MECHANISM OF ACTION C. Sanchez , J. Zappia , Y. Dierckxsens , J.-P. Delcour , Y. Henrotin . 1Univ. of Li ege, liege, Belgium; 2 Tilman, Baillonville, Belgium; Orthopedic Dept., Bois de l'Abbaye Hosp. center, liege, Belgium Purpose: Boswellia serrata extract (BSE) and curcumin are used to relief symptoms in osteoarthritis (OA). This study aims to better understand the mode of action of these compounds on OA chondrocytes in vitro. Methods: Therapeutic plasmatic concentrations of the different components of BSE correspond to an in vitro range from 25 to 100 mg/ml of total BSE (100 mg/ml of BSE corresponds to 9.2 mM of 11-keto-b-boswellic acid (KBA), 5.2 mMof acetylKBA, 22 mMde aBA, 34 mMde bBA, 4.4 mM de acetylaBA and 13.2 acetyl bBA), and between 2 to 10 mM for bioavaibility-increased curcumin. BSE (5-100 mg/ml) and curcumin (0.04 to 4 mg/ml corresponding to 0.1 to 10 mM) were tested separately on primary chondrocytes from 3 OA patients. Lactate Deshydrogenase LDH, nitrite (NO2), interleukin (IL)-6 and Growth Differentiation Factor (GDF)15 were quantified in 72h-treated supernatant using enzyme activity, Griess reaction and ELISAs, respectively. Results: No mortality was observed at the tested concentrations. BSE and curcumin both decreased concentration-dependently NO2 and IL-6 production, and increased GDF15 production. For NO2 production, the decrease was observed from 0.2 mg/ml of curcumin and 10 mg/ml of BSE. For IL-6 production, the decrease was observed from 1 mg/ml for curcumin and 10 mg/ml for BSE. For GDF-15, the increase was observed from 2 mg/ml for curcumin and 50 mg/ml for BSE. Maximal effect was observed at 4 mg/ml for curcumin: -67% NO2 (p<0.0001), -71% IL-6 (p1⁄40.0001) andþ80% GDF15 (p<0.0001) and at 100 mg/ml for BSE: -40% NO2 (p1⁄40.0003), -70% IL-6 (p1⁄40.0003) andþ73% for GDF15 (p1⁄40.0017). Conclusions: At therapeutic plasmatic concentrations, BSE and curcumin decreased the production of NO2 and IL-6, two inflammatory mediators. Furthermore, BSE and curcumin enhanced GDF-15 production, an anti-inflammatory growth factor. GDF15 was first identified as Macrophage inhibitory cytokine-1 or NSAID-activated gene-1 (by a prostanoid-independent manner), and is known as a regulator of inflammatory, cell repair and apoptosis pathways. GDF-15 has proapoptotic and anti-tumorigenic activity in vitro and in vivo. It could represent a new pathway explaining the beneficial effects of BSE and the curcumin on synovium inflammation and cartilage degradation. 166 EVALUATING CYTOKINES AS BIOMARKERS FOR TRAPEZIOMETACARPAL OSTEOARTHRITIS A. Ratneswaran, J. Rockel, K. Shestopaloff, D. Antflek, M. Kapoor, H. Baltzer. Arthritis Res. Program, Univ. Hlth.Network, Toronto, ON,