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DOI: 10.1055/s-2003-818008
Demethylbellidifolin Inhibits Adhesion of Monocytes to Endothelial Cells via Reduction of Tumor Necrosis Factor alpha and Endogenous Nitric Oxide Synthase Inhibitor Level
This study was supported by a grant from the Provincial Natural Science Foundation of Hunan, China, No. 02jjy2046Publikationsverlauf
Received: May 7, 2003
Accepted: August 30, 2003
Publikationsdatum:
29. Januar 2004 (online)

Abstract
The effect of demethylbellidifolin (DMB), a major compound of Swertia davidi Franch, on the adhesion of monocytes to endothelial cells induced by oxidized low-density lipoprotein (ox-LDL) was studied. Adhesion of monocytes to endothelial cells was induced by treatment with ox-LDL (100 μg/mL) for 48 h. Levels of tumor necrosis factor-α (TNF-α) and asymmetric dimethylarginine (ADMA, an endogenous inhibitor of NOS) in conditioned medium and the activity of dimethylarginine dimethylaminohydrolase (DDAH) in endothelial cells were measured. DMB (3 or 10 μmol/L) significantly inhibited the adhesion of monocytes to endothelial cells, attenuated an increase in levels of TNF-α and ADMA, and a decrease in the activity of DDAH by ox-LDL. The present results suggest that DMB inhibits the increased adhesion of monocytes to endothelial cells induced by ox-LDL, and that the effect of DMB is related to reduction of the ADMA concentration via reduction of TNF-α production in cultured endothelial cells treated with ox-LDL.
References
- 1 Böger R H, Bode-Böger S M, Szuba A, Tsao P S, Chan J R, Tangphao O, Blaschke T F, Cooke J P. Asymmetric dimethylarginine: a novel risk factor for endothelial dysfunction: its role in hypercholesterolemia. Circulation. 1998; 98 1842-7
- 2 Yu X J, Li Y J, Xiong Y. Increase of an endogenous inhibitor of nitric oxide synthesis in serum of high cholesterol fed rabbits. Life Sci. 1994; 54 753-8
- 3 Rus H, Niculescu F, Vlaicu R. Tumor necrosis factor-α in human arterial wall with atherosclerosis. Atherosclerosis. 1991; 89 247-54
- 4 Tanaka H, Sukhova G, Schwartz D, Libby P. Proliferating arterial smooth muscle cells after balloon injury express TNF-α but not interleukin-1 or basic fibroblast growth factor. Arterioscler Thromb Vasc Biol. 1996; 16 12-18
- 5 Chen Y H, Lin S J, Chen J W, Ku H H, Chen Y L. Magnolol attenuates VCAM-1 expression in vitro in TNF-alpha-treated human aortic endothelial cells and in vivo in the aorta of cholesterol-fed rabbits. Br J Pharmacol. 2002; 135 37-47
- 6 Ito A, Tsao P S, Adimoolam S, Kimoto M, Ogawa T, Cooke J P. Novel mechanism for endothelial dysfunction: dysregulation of dimethylarginine dimethylaminohydrolase. Circulation. 1999; 99 3092-5
- 7 Peres V, Nagem T J, De oliveira F F. Tetraoxygenated naturally occurring xanthones. Phytochemistry. 2000; 55 683-710
- 8 Madan B, Singh I, Kumar A, Prasad A K, Raj H G, Parmar V S. Xanthones as inhibitors of microsomal lipid peroxidation and TNF-alpha induced ICAM-1 expression on human umbilical vein endothelial cells (HUVECs). Bioorg Med Chem. 2002; 10 3431-6
- 9 Jiang D J, Jiang J L, Tan G S, Du Y H, Xu K P, Li Y J. Protective effects of daviditin A against endothelial damage induced by lysophosphatidylcholine. N-S Arch Pharmacol;. 2003; 367 600-6
- 10 Cooke J P. Does ADMA cause endothelial dysfunction?. Arterioscler Thromb Vasc Biol. 2000; 20 2032-7
Yuan-Jian Li, MD
Department of Pharmacology
School of Pharmaceutical Sciences
Central South University
Xiang-Ya Road #88
Changsha 410078
P. R. China
Telefon: +86-731-4805441
Fax: +86-731-2650442
eMail: yuan_jianli@yahoo.com