Chondroitin sulfate inhibits the nuclear translocation of nuclear factor-κB in interleukin-1β-stimulated chondrocytes

摘要: Chondroitin sulfate is referred as a symptomatic slow-acting drug for osteoarthritis because it improves articular function, and reduces joint swelling effusion. In addition, chondroitin prevents space narrowing of the knee. We hypothesized that anti-inflammatory effect associated to decrease in activation mitogen-activated protein kinases (MAPK) transcription factors nuclear factor-kappaB (NF-kappaB) activator protein-1 (AP-1). Cultured rabbit chondrocytes were stimulated with interleukin-1beta (IL-1beta) presence sulfate. Nuclear translocation NF-kappaB AP-1, nitrite concentrations (as an index nitric oxide) was assessed 48 hr later. The on IL-1beta extracellular signal-regulated kinase 1/2 (Erk1/2) p38MAPK documented by immunoblot. sodium nitroprusside-induced apoptosis evaluated terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling assay. reduced IL-1beta-induced translocation, but not AP-1 decreased phosphorylation Erk1/2 abrogated phosphorylation, did prevent increase nitrite. Finally, chondrocytes. These results suggest some biological activities may be reduction transactivation NF-kappaB.