Planta Med 2005; 71(9): 829-834
DOI: 10.1055/s-2005-871296
Original Paper
Pharmacology
© Georg Thieme Verlag KG Stuttgart · New York

Endothelial Nitric Oxide Production Stimulated by the Bioflavonoid Chrysin in Rat Isolated Aorta

Inmaculada Concepción Villar1 , 3 , Rocío Vera1 , 3 , Milagros Galisteo1 , Francisco O’Valle2 , Miguel Romero1 , Antonio Zarzuelo1 , Juan Duarte1
  • 1Departamento de Farmacología, Facultad de Farmacia, Universidad de Granada, Granada, Spain
  • 2Departamento de Patología, Facultad de Medicina, Universidad de Granada, Granada, Spain
  • 3I. C. Villar and R. Vera contributed equally to this work
Further Information

Publication History

Received: November 11, 2004

Accepted: April 25, 2005

Publication Date:
19 August 2005 (online)

Preview

Abstract

In the present study, the effects of the bioflavonoid chrysin (5,7-dihydroxyflavone) were analysed on nitric oxide (NO) production from vascular endothelium. In aortic rings, incubation with chrysin or acetylcholine (both at 10 μM) increased L-NAME-sensitive endothelial NO release as measured using the fluorescent probe 4,5-diaminofluorescein diacetate (DAF-2 DA). Moreover, chrysin increased cGMP accumulation only in aortic rings with endothelium. However, at this concentration, chrysin had no effect either on basal or on NADPH-stimulated vascular superoxide production. Moreover, at this low concentration, chrysin, similar to acetylcholine, induced aortic relaxation, which was abolished by both endothelial deprivation and NO synthase inhibition. Endothelium-dependent relaxation induced by chrysin was unaltered by removal of extracellular calcium and incubation with the intracellular calcium chelator BAPTA, while the phosphatidylinositol (PI)-3 kinase inhibitor wortmannin suppressed the endothelial dependence. In conclusion, chrysin stimulated NO release from endothelial cells leading to vascular cGMP accumulation and subsequent endothelium dependent aortic relaxation. Chrysin-stimulated NO release is calcium independent and possibly mediated via PI3-kinase.

References

J. Duarte

Departamento de Farmacología

Facultad de Farmacia

Universidad de Granada

18071 Granada

Spain

Phone: +34-958-244-088

Fax: +34-958-248-964

Email: jmduarte@platon.ugr.es