Panax Quinquefolium L. Inhibits Thrombin-Induced Endothelin Release In Vitro

Author:

Yuan Chun-Su12,Attele Anoja S.2,Wu Ji An2,Lowell Tasha K.2,Gu Zhenlun3,Lin Yuan4

Affiliation:

1. Committee on Clinical Pharmacology, Pritzker School of Medicine, The University of Chicago, Chicago, lL 60637, U.S.A.

2. Department of Anesthesia and Critical Care, Pritzker School of Medicine, The University of Chicago, Chicago, lL 60637, U.S.A.

3. Department of Pharmacology, Suzhou Medical College, Suzhou 215007, China

4. Marco Polo Technologies, Bethesda, MD 20817, U.S.A.

Abstract

Endothelial cell damage is considered to be the initial step in the genesis of thrombosis and arteriosclerosis, the common precursors of cardiovascular disorders. In this study, we evaluated the protective effects of American ginseng or Panax quinquefolium L. extracts on endothelial cell injury, and investigated effects of ginseng extracts on thrombin-induced endothelin release using cultured human umbilical vein endothelial cells. We observed that when endothelial cells pretreated with 1, 10, and 100 μg/ml of Panax quinquefolium L. extracts were incubated for 4 and 24 hr with thrombin, the concentration of endothelin was significantly decreased in a concentration dependent, time related manner (at 4 hr, IC50 = 5.1 μg/ml; at 24 hr, IC50 = 6.2 μg/ml). We further evaluated the effects of NG-nitro-L-arginine (NLA), a nitric oxide (NO) synthetase inhibitor, on the activity of Panax quinquefolium L. extracts. Following pretreatment of cultured endothelial cells with NLA, the inhibition of thrombin-induced endothelin release by Panax quinquefolium L. was significantly reduced (P < 0.05). This result suggests that the pharmacological action of Panax quinquefolium L. is, at least partially, due to NO release. Our data demonstrate that American ginseng may play a therapeutic role in facilitating the hemodynamic balance of vascular endothelial cells.

Publisher

World Scientific Pub Co Pte Lt

Subject

Complementary and alternative medicine,General Medicine

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