4.7 Article

Meroterpenoid-Rich Fraction of the Ethanol Extract of Sargassum Serratifolium Suppresses Collagen-Induced Rheumatoid Arthritis in DBA/1J Mice Via Inhibition of Nuclear Factor κB Activation

Journal

MOLECULAR NUTRITION & FOOD RESEARCH
Volume 64, Issue 3, Pages -

Publisher

WILEY
DOI: 10.1002/mnfr.201900373

Keywords

collagen-induced arthritis; inflammatory suppression; NF-kappa B; rheumatoid arthritis; Sargassum serratifolium

Funding

  1. Ministry of Oceans and Fisheries, Republic of Korea
  2. National Research Foundation of Korea [2019R111A3A01159690]
  3. National Research Foundation of Korea (NRF) [2018R1D1A1B07049801]
  4. National Research Foundation of Korea [2018R1D1A1B07049801] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Scope Rheumatoid arthritis (RA) is an autoimmune disorder related to the inflammation of cartilage due to the infiltration of inflammatory cells. Sargassum serratifolium, a brown alga, possesses strong anti-inflammatory activities. Methods and Results The effect of meroterpenoid-rich fraction from the ethanol extract of S. serratifolium (MES) on RA and its underlying mechanisms on the inhibition of RA using a collagen-induced arthritis (CIA) mouse model are examined. The results show that MES ameliorates paw swelling and reduces the arthritis score. MES considerably decreases the secretion of pro-inflammatory cytokines in the serum and joint tissue of mice. Histopathological analysis demonstrates that MES strongly inhibited bone damage and inflammatory cell intrusion in the joint tissue. The expression of inflammatory enzymes and adhesion molecules is significantly inhibited in the serum and joint tissue of MES-fed mice. In addition, MES downregulates the nuclear factor kappa B (NF-kappa B) signaling pathway by suppressing the phosphorylation of protein kinase B, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinases. Conclusions MES supplementation remarkably reduces inflammatory response in CIA mouse model. These results indicate that MES can be used as a pharmaceutical agent against RA.

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