Vascular effects of a soy leaves (Glycine max) extract and kaempferol glycosides in isolated rat carotid arteries.
We have recently purified genistin, and six kaempferol glycosides from a soy leaves ( Glycine max L. Merr.) butanol extract. Here we report the vascular effects of the extract and purified genistin and kaempferol glycosides on contractions induced by different constricting agonists in isolated rat carotid arteries. The butanol extract relaxed artery rings preconstricted by 9,11-dideoxy-11alpha,9alpha-epoxy-methanoprostaglandin F 2 alpha (U46619) or [5 Z,9alpha,11alpha,13 E,15 S]-9,11,15-trihydroxyprosta-5,13-dienoic acid (PGF 2 alpha ) in a dose-dependent manner and this effect was independent of the presence of endothelium. The extract also inhibited the concentration-dependent contraction to U46619 with a slight reduction of the maximal response. The extract produced partial relaxation of both phenylephrine-preconstricted endothelium-intact and -denuded rings. In contrast, the extract had no effect on the contractile response to 50 mM extracellular K (+). None of the six kaempferol glycosides affected vessel tension induced by U46619. A mixture of kaempferol glycosides prepared according to their relative composition in the extract had no effect either. However, kaempferol relaxed U46619- and high K (+)-contracted rings to the same extent. Endothelium played no role in kaempferol-induced relaxation. Genistein induced concentration-dependent relaxation and this effect was attenuated in the endothelium-denuded rings. Genistin caused a smaller relaxant effect. The present results indicate that a butanol extract from soy leaves causes endothelium-independent relaxation in rat carotid artery rings. Kaempferol glycosides, accounting for approximately 48 % of the extract in weight, are not the ingredients responsible for the extract-induced relaxation. Genistein and genistin also caused relaxation, however, the dose range is beyond that of the extract causing relaxation.
Ho
Hing Man
HM
Department of Biochemistry, Chinese University of Hong Kong, Shatin, NT, China.
Chen
Ruoyun
R
Huang
Yu
Y
Chen
Zhen Yu
ZY
D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid / Q000494:pharmacology; D000818:Animals; D002339:Carotid Arteries / Q000187:drug effects* / Q000502:physiology; D015237:Dinoprost / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000502:physiology; D005419:Flavonoids; D019833:Genistein / Q000494:pharmacology; D007529:Isoflavones / Q000494:pharmacology; D044949:Kaempferols; D008297:Male; D010936:Plant Extracts / Q000494:pharmacology*; D018515:Plant Leaves / Q000737:chemistry; D011188:Potassium / Q000494:pharmacology; D011453:Prostaglandins / Q000494:pharmacology; D011794:Quercetin / Q000031:analogs & derivatives* / Q000737:chemistry / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013025:Glycine max; D014661:Vasoconstriction / Q000187:drug effects*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D005419:Flavonoids; D007529:Isoflavones; D044949:Kaempferols; D010936:Plant Extracts; D011453:Prostaglandins; D014662:Vasoconstrictor Agents; C040641:genistin; C006552:kaempferol; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D011794:Quercetin; D015237:Dinoprost; D019833:Genistein; D011188:Potassium