Chondroitin sulfate A (CSA) is a glycosaminoglycan.[1] It can be biosynthetically polymerized in a variety of species and serve as structural components in cartilage when tethered to extracellular proteins. CSA (0.5 or 1 mg/ml) reduces LPS-induced decreases in viability, as well as LPS-induced increases in Tnf-α, Il-1β, Il-6, Ifn-γ, inducible nitric oxide synthase (iNOS), and matrix metalloproteinase-1 (Mmp-1) levels, nitric oxide (NO) production, and NF-κB activity in primary mouse chondrocytes.[2] Extracellular CSA is required for P. falciparum-infected erythrocytes to adhere to the endothelium in the brain and placenta and avoid immune detection.[3] In vivo, CSA (30, 60, or 120 mg/kg per day) reduces arthritis incidence and joint swelling, decreases 8-isoprostane levels in articular cartilage cells, and increases IκBα levels in cartilage cell cytoplasm in a mouse model of collagen-induced arthritis.[4]
References:
[1].Kwok, J.C.F., Warren, P., and Fawcett, J.W.Chondroitin sulfate: A key molecule in the brain matrixInt. J. Biochem. Cell Biol.44(4)582-586(2012).
[2].Campo, G.M., Avenoso, A., Campo, S., et al.Glycosaminoglycans modulate inflammation and apoptosis in LPS-treated chondrocytesJ. Cell. Biochem.106(1)83-92(2009).
[3].Reeder, J.C., Cowman, A.F., Davern, K.M., et al.The adhesion of Plasmodium falciparum-infected erythrocytes to chondroitin sulfate A is mediated by P. falciparum erythrocyte membrane protein 1Proc. Natl. Acad. Sci. U.S.A.96(9)5198-5120(1999).
[4].Campo, G.M., Avenoso, A., Campo, S., et al.Chondroitin-4-sulphate inhibits NF-kB translocation and caspase activation in collagen-induced arthritis in miceOsteoarthritis Cartilage16(12)1474-1483().