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논문 기본 정보

자료유형
학술저널
저자정보
서정우 (국립부경대학교) Jo Sung-Han (The Center for Marine Integrated Biomedical Technology (BK21 PLUS), Pukyong National University) Kim Seon-Hwa (The Center for Marine Integrated Biomedical Technology (BK21 PLUS), Pukyong National University) Choi Byeong-Hoon (Department of Industry 4.0 Convergence Bionics Engineering, Pukyong National University) Cho Hongsik (Department of Orthopedic Surgery and Biomedical Engineering, University of Tennessee Health Science Center-Campbell Clinic) Yoo James J. (Wake Forest Institute for Regenerative Medicine, Wake Forest School of Medicine) Park Sang-Hyug (Department of Biomedical Engineering, Pukyong National University)
저널정보
한국조직공학과 재생의학회 조직공학과 재생의학 조직공학과 재생의학 제21권 제2호
발행연도
2024.2
수록면
209 - 221 (13page)
DOI
10.1007/s13770-023-00587-0

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BACKGROUND: Rheumatoid arthritis (RA) is characterized by chronic inflammation and joint damage. Methotrexate (MTX), a commonly used disease-modifying anti-rheumatic drug (DMARD) used in RA treatment. However, the continued use of DMARDs can cause adverse effects and result in limited therapeutic efficacy. Cartilage extracellular matrix (CECM) has anti-inflammatory and anti-vascular effects and promotes stem cell migration, adhesion, and differentiation into cartilage cells. METHODS: CECM was assessed the dsDNA, glycosaminoglycan, collagen contents and FT-IR spectrum of CECM. Furthermore, we determined the effects of CECM and MTX on cytocompatibility in the SW 982 cells and RAW 264.7 cells. The anti-inflammatory effects of CECM and MTX were assessed using macrophage cells. Finally, we examined the in vivo effects of CECM in combination with MTX on anti-inflammation control and cartilage degradation in collagen-induced arthritis model. Anti-inflammation control and cartilage degradation were assessed by measuring the serum levels of RA-related cytokines and histology. RESULTS: CECM in combination with MTX had no effect on SW 982, effectively suppressing only RAW 264.7 activity. Moreover, anti-inflammatory effects were enhanced when low-dose MTX was combined with CECM. In a collagen-induced arthritis model, low-dose MTX combined with CECM remarkably reduced RA-related and pro-inflammatory cytokine levels in the blood. Additionally, low-dose MTX combined with CECM exerted the best cartilage-preservation effects compared to those observed in the other therapy groups. CONCLUSION: Using CECM as an adjuvant in RA treatment can augment the therapeutic effects of MTX, reduce existing drug adverse effects, and promote joint tissue regeneration.

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