|
KMID : 0043320070300101318
|
|
Archives of Pharmacal Research
2007 Volume.30 No. 10 p.1318 ~ p.1335
|
|
|
Anti-Inflammatory Mechanisms of Apigenin: Inhibition of Cyclooxygenase-2 Expression, Adhesion of Monocytes to Human Umbilical Vein Endothelial Cells, and Expression of Cellular Adhesion Molecules
|
|
Lee Je-Hyuk
Zhou Hong-Yu
Kim Yeong-Shik
Lee Yong-Soo
Jeong Choon-Sik
|
|
|
Abstract
|
|
|
|
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-α (TNF-α)-induced adhesion of monocytes to HUVEC monolayer. Apigenin significantly suppressed the TNF-α-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
|
|
|
KEYWORD
|
|
|
Apigenin, Collagenase, Hyaluronidase, Nitric oxide, COX-2, Adhesion, VCAM-1, ICAM-1, E-selectin
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
  
|