A crude extract from Acanthopanax senticosus (AS) has drawn increased attention because of its potentially beneficial activities, including anti-fatigue, anti-stress, anti-gastric-ulcer, and immunoenhancing effects. We previously reported that AS crude extract exerts anti-inflammatory
activity through blockade of monocytic adhesion to endothelial cells. However, the underlying mechanisms remained unknown, and so this study was designed to investigate the pathways involved. It was confirmed that AS extract inhibited lipopolysaccharide (LPS)-induced adhesion of monocytes
to endothelial cells, and we found that whole extract was superior to eleutheroside E, a principal functional component of AS. A series of PCR experiments revealed that AS extract inhibited LPS-induced expression of genes encoding lymphocyte function-associated antigen-1 (LFA-1) and macrophage-1
antigen (Mac-1) in THP-1 cells. Consistently, protein levels and cell surface expression of LFA-1 and Mac-1 were noticeably reduced upon treatment with AS extract. This inhibitory effect was mediated by the suppression of LPS-induced degradation of IκB-α, a known inhibitor of nuclear
factor-κB (NF-κB). In conclusion, AS extract exerts anti-inflammatory activity via the suppression of LFA-1 and Mac-1, lending itself as a potential therapeutic galenical for the prevention and treatment of various inflammatory diseases.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Article Media
Acanthopanax senticosus extract;
extrait d’Acanthopanax senticosus
Document Type: Research Article
Department of Molecular Biology & Institute of Nanosensor and Biotechnology, Dankook University, 126, Jukjeon-dong, Suji-gu, Yongin-si, Gyeonggi-do 448-701, Korea.
Cardiovascular Research Institute, University of Vermont, 208 South Park Drive, Colchester, VT 05446, USA.
Department of Life Systems, Sookmyung Women’s University, 52 Hyochangwon-gil, Yongsan-gu, Seoul 140-742, Korea.
Publication date: January 1, 2014
More about this publication?