The aim of this study was to clarify the anti-inflammatory mechanism of apigenin. Apigenin inhibited the collagenase activity involved in rheumatoid arthritis (RA) and suppressed lipopolysaccharide (LPS)-induced nitric oxide (NO) production in a dose dependent manner in RAW 264.7 macrophage cells. Pretreatment with apigenin also attenuated LPS-induced cyclooxygenase-2 (COX-2) expression. In addition, apigenin profoundly reduced the tumor necrosis factor-alpha (TNF-alpha)-induced adhesion of monocytes to HUVEC monolayer. Apigenin significantly suppressed the TNF-alpha-stimulated upregulation of vascular cellular adhesion molecule-1 (VCAM-1)-, intracellular adhesion molecule-1 (ICAM-1)-, and E-selectin-mRNA to the basal levels. Taken together, these results suggest that apigenin has significant anti-inflammatory activity that involves blocking NO-mediated COX-2 expression and monocyte adherence. These results further suggest that apigenin may be useful for therapeutic management of inflammatory diseases.

No abstract

No abstract

Chondroitin sulfate (CS) is a glycosaminoglycan, which is composed of an alternating sequence of sulfated and/or unsulfated residue of D-glucuronic acid (GlcA) and D-N-acetylgalactosamine (GalNAc) linked by b(1→3) and b(1→4) bonds.1) CS is a major class of glycosaminoglycans required for the formation of proteoglycans found in the joint cartilage. It has been well established that basic damage to the arthritic cartilage involves the alteration of proteoglycans and collagen fibers.