Open AccessImmunomodulatory and anti‐inflammatory effects of chondroitin sulphate
Author(s) -
du Souich Patrick,
García Antonio G.,
Vergés Josep,
Montell Eulàlia
Publication year - 2009
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2009.00826.x
Subject(s) - inflammation , p38 mitogen activated protein kinases , chemistry , proinflammatory cytokine , mechanism of action , tumor necrosis factor alpha , signal transduction , kinase , arthritis , protein kinase a , pharmacology , medicine , immunology , cancer research , endocrinology , biochemistry , in vitro
• Biochemistry of chondrotin sulphate • Mechanism of action of chondroitin sulphate ‐ Effect of chondroitin sulphate on the chondrocyte ‐ Effect of chondroitin sulphate on the synovial membrane ‐ Effect of chondroitin sulphate on subchondral bone• Human use of chondroitin sulphate ‐ Chondrotin sulphate in osteoarthritis ‐ Chondrotin sulphate in psoriasis ‐ Chondrotin sulphate in atherosclerosis ‐ Chondroitin sulphate in IBD ‐ Chondroitin sulphate in degenerative diseases of the central nervous system (CNS) ‐ Other autoimmune diseases that may benefit from chondroitin sulphate• ConclusionsChondroitin sulphate (CS) is a natural glycosaminoglycan present in the extracellular matrix and is formed by the 1–3 linkage of D‐glucuronic acid to N‐acetylgalactosamine. In chondrocytes, CS diminishes interleukin‐1 p (IL‐1p)‐induced increases in p38 mitogen‐activated protein kinase (p38MAPK) and signal‐regulated kinase 1/2 (Erk1/2) phosphorylation, and decreases nuclear factor‐KB (NF‐kB) nuclear translocation and as a consequence, reduces the formation of pro‐inflammatory cytokines, IL‐1 p and TNF‐a, and pro‐inflammatory enzymes, such as phospholipase A2 (PLA2), cyclooxygenase 2 (COX‐2) and nitric oxide synthase‐2 (NOS‐2). The mechanism of action of CS explains its beneficial effect on the cartilage, synovial membrane and subchondral bone. On the other hand, in vivo , CS given orally prevents hepatic NF‐kB nuclear translocation, suggesting that systemic CS may elicit an anti‐inflammatory effect in many tissues besides the articulation. There is preliminary evidence showing that in human beings, CS may be of benefit in other diseases where inflammation is an essential marker, such as psoriasis and atherosclerosis. The review of the literature suggest that CS might also be of interest for the treatment of other diseases with an inflammatory and/or autoimmune character, such as inflammatory bowel disease, degenerative diseases of the central nervous system and stroke, multiple sclerosis and other autoimmune diseases.