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AB0112 CSD-125, A Soft Coral-Derived Anti-Inflammatory Compound, Attenuates Joint Destruction via Osteoclastogenesis in A Type II Collagen-Induced Arthritis Rat Model
  1. Y.-Y. Lin1,
  2. S.-C. Lin2,
  3. H.-P. Li2,
  4. Y.-H. Jean2,
  5. Z.-H. Wen1
  1. 1Marine Biomedical Laboratory and Center for Translational Biopharmaceuticals, Department of Marine Biotechnology and Resources, National Sun Yat-Sen University, Kaohsiung
  2. 2Department of Orthopaedic Surgery, Ping-Tung Christian Hospital, Ping-Tung, Taiwan, Province of China


Background Rheumatoid arthritis (RA) is a common rheumatic disease that is characterized by synovial inflammation of the synovial tissue that lines the joints [1]. Osteoclasts become active and mature by stimulation of inflammatory cytokines such as macrophage colony-stimulating factor (M-CSF), interleukin-1b (IL-1b), interleukin-17A (IL-17A), and tumor necrosis factor-a (TNF-a), and also play a critical role in the bone destruction in RA [2]. Soft corals have been considered an important resource of anti-inflammatory agents that may be beneficial for treating inflammatory diseases [3–5].

Objectives In this present study, we investigated the therapeutic effects of CSD-125, a soft coral-derived compound in type II collagen-induced arthritis (CIA), via its role in the anti-osteoclastic pathway.

Methods A rat model of CIA was established, and knee joint tissue destruction was evaluated in rats treated with and without CSD-125 by the RA index, histopathology, immunohistochemistry, and western blotting. We also analyzed the level of pro-inflammatory cytokines such as M-CSF and IL-17A in the blood serum.

Results The results demonstrated that CSD-125 significantly attenuated CIA-induced RA progression in rats. CSD-125 also decreased the expression of osteoclast-related proteins, including cathepsin K, matrix metalloproteinases-9, matrix metalloproteinases-2, cluster of differentiation molecule 11B, nuclear factor of activated T cells, cytoplasmic 1 (NFATC 1), and triggering receptor on myeloid cells 2 (TREM 2), in multinucleated cells. Moreover, CSD-125 reduced the number of cells showing positive expression of IL-17A, IL-1b, and TNF-a, phospho-extracellular signal-regulated kinases (p-ERK), phospho-c-Jun N-terminal kinase (p-JNK), and phospho-p38 (p-P38) in the synovial tissue of CIA-rats. The levels of M-CSF and IL-17A also decreased following administration of CSD-125 to CIA-rats.

Conclusions These results provide strong support that CSD-125 could attenuate the joint destruction in type II CIA, likely through inhibition of osteoclast activation.

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  2. Shiozawa, S., et al., Pathogenesis of joint destruction in rheumatoid arthritis. Arch Immunol Ther Exp (Warsz), 2011. 59(2): p. 89–95.

  3. Blunt, J.W., et al., Marine natural products. Nat Prod Rep, 2015. 32(2): p. 116–211.

  4. Lin, Y.Y., et al., A soft coral-derived compound, 11-epi-sinulariolide acetate suppresses inflammatory response and bone destruction in adjuvant-induced arthritis. PLoS One, 2013. 8(5): p. e62926.

  5. Gonzalez, Y., et al., Marine Diterpenoids as Potential Anti-Inflammatory Agents. Mediators Inflamm, 2015. 2015: p. 263543.

Acknowledgement This study was supported by grants from the Ministry of Science and Technology (MOST 103–2628-B-110–002-MY3 and MOST 104–2325-B-110–001) of Taiwan and Pingtung Christian Hospital, Taiwan.

Disclosure of Interest None declared

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