SEARCH · PubMed Health

Results for “Kaempferols”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed2004

Absorption of kaempferol from endive, a source of kaempferol-3-glucuronide, in humans.

OBJECTIVE: To determine the absorption, excretion and metabolism of kaempferol in humans. DESIGN: A pharmacokinetic study of kaempferol from endive over 24 h. SUBJECTS: Four healthy males and four healthy females. RESULTS: Kaempferol, from a relatively low dose (9 mg), was absorbed from endive with a mean maximum plasma concentration of 0.1 microM, at a time of 5.8 h, indicating absorption from the distal section of the small intestine and/or the colon. Although a 7.5-fold interindividual variation between the highest and lowest maximum plasma concentration was observed, most individuals showed remarkably consistent pharmacokinetic profiles. This contrasts with profiles for other flavonoids that are absorbed predominantly from the large intestine (eg rutin). An average of 1.9% of the kaempferol dose was excreted in 24 h. Most subjects also showed an early absorption peak, probably corresponding to kaempferol-3-glucoside, present at a level of 14% in the endive. Kaempferol-3-glucuronide was the major compound detected in plasma and urine. Quercetin was not detected in plasma or urine indicating a lack of phase I hydroxylation of kaempferol. CONCLUSIONS: Kaempferol is absorbed more efficiently than quercetin in humans even at low oral doses. The predominant form in plasma is a 3-glucuronide conjugate, and interindividual variation in absorption and excretion is low, suggesting that urinary kaempferol could be used as a biomarker for exposure.

Administration, Oral↗

PubMed2003

Radiolysis of kaempferol in water/methanol mixtures. Evaluation of antioxidant activity of kaempferol and products formed.

Oxidative reaction between hydroxymethyl radical ((*)CH(2)OH) and kaempferol, in methanol and methanol/water mixtures, was studied by gamma-radiolysis using a (60)Co source. Radiolysis was performed with concentrations and doses ranging from 5 x 10(-)(5) M to 5 x 10(-)(3) M and from 0.5 kGy to 14 kGy, respectively. Kaempferol degradation was followed by HPLC. Results showed that (*)CH(2)OH reacts with kaempferol at the 3-OH group and produces two depsides (K1 and K2) and other products including K3. K1, K2, and K3 were identified by NMR, LC-MS, and HRMS. The kaempferol degradation pathway leading to the K1, K2, and K3 formation is proposed. It was observed that the more water concentration in the irradiation medium increases, the more K2 concentration increases. Comprehension of food preservation is not clear because many phenomena occurring during irradiation are not established. Radiolysis of kaempferol in water/methanol mixtures helps to elucidate the phenomenon and it is possible that during the treatment of nutriments by gamma-irradiation, a series of products such as depside K2 could be formed. Antioxidant properties of kaempferol radiolysis products were evaluated according to their capacity to decrease the EPR DPPH (1,1-diphenyl-2-picrylhydrazil) signal and to inhibit superoxide radicals formed by the enzyme reaction "xanthine + xanthine oxidase".

Antioxidants↗

PubMed1997

Involvement of rat cytochrome 1A1 in the biotransformation of kaempferol to quercetin: relevance to the genotoxicity of kaempferol.

Kaempferol is a flavonoid widely distributed in edible plants and has been shown to be genotoxic to V79 cells in the absence of external metabolizing systems. The presence of an external metabolizing system, such as rat liver homogenates (S9 mix), leads to an increase in its genotoxicity, which is attributed to its biotransformation to the more genotoxic flavonoid quercetin, via the cytochrome P450 (CYP) mono-oxygenase system. In the present work we investigated the mechanisms of the genotoxicity of kaempferol further. Special attention has been given to the role of CYP in the genotoxicity of this flavonoid. We studied the induction of mutations in Salmonella typhimurium TA98 in the presence and in the absence of S9 mix and the induction of chromosomal aberrations (CAs) and micronuclei (MN) by kaempferol in V79 cells in the presence and in the absence of S9 mix. To evaluate the role of different CYP in the biotransformation of kaempferol we studied the induction of CAs and MN in V79 cells genetically engineered for the expression of rat CYP 1A1, 1A2 and 2B1. In addition we performed CYP inhibition studies using the above-mentioned indicators and high performance liquid chromatography (HPLC) analysis. The results obtained in this work suggest that rat CYP 1A1 is, among the cytochromes studied, the one that plays the major role in the transformation of kaempferol into quercetin. The relevance of these findings to the human situation is discussed.

Animals↗

PubMed2000

Cytotoxic activity of kaempferol glycosides against human leukaemic cell lines in vitro.

Two kaempferol coumaroyl glycosides (i.e. platanoside and tiliroside) isolated from the methanolic extract of Platanus orientalis L. buds, were examined for their in vitro cytotoxic activity against a panel of human leukaemic cell lines. Platanoside (1) exhibited cytotoxic activity against most of the cell lines tested, while tiliroside (2) was active against two of the nine tested cell lines. Compound 1, was examined for its effect on the uptake of [(3)H]thymidine as a marker of DNA synthesis. Kaempferol was used as a control.

Antineoplastic Agents, Phytogenic↗

PubMed2006

Biphasic effects of kaempferol on the estrogenicity in human breast cancer cells.

Dietary flavonoids have attracted a great deal of attention as agents for preventing estrogen-related diseases, such as postmenopausal symptoms, and for reducing the risk of estrogen-dependent cancer. Kaempferol is one of the most commonly found dietary phytoestrogen. The aim of this study was to investigate the estrogenic and/or antiestrogenic effect of kaempferol, which can confirm its potency as a preventive agent against estrogen-related diseases. Kaempferol has both estrogenic and antiestrogenic activity, which are biphasic response on estrogen receptor. The estrogenic activity of kaempferol induced via ER-mediated pathway depending on E2 concentration (< or = 10(-12) M). Kaempferol (10(-5) M) also caused antiproliferative effect on MCF-7 cell in the presence of E2 (10(-11) M) and restored to the addition of excess E2 (10(-7) M), which confirms that antiproliferation of kaempferol was induced via ER-dependent pathway. However, at 10(-4) M, concentration higher than the concentrations at which the estrogenic effects of kaempferol are detected (10(-5) M), kaempferol induced strong antiproliferative effect, but were unaffected by the addition of excess E2 (10(-7) M) indicating that kaempferol exerts antiproliferation via ER-independent pathway. In particular, kaempferol blocked the focus formation induced by E2, which confirms that kaempferol might inhibit the malignant transformation caused by estrogens. Therefore, we suggested that kaempferol might regulate a suitable level of estrogenic activity in the body and is expected to have potential beneficial effects in preventing estrogen imbalance diseases (breast cancer, osteoporosis, cardiovascular disease and etc.).

Breast Neoplasms↗

PubMed2005

Protective and detrimental effects of kaempferol in rat H4IIE cells: implication of oxidative stress and apoptosis.

Flavonoids are ubiquitous substances in fruits and vegetables. Among them, the flavonol kaempferol contributes up to 30% of total dietary flavonoid intake. Flavonoids are assumed to exert beneficial effects on human health, e.g., anticancer properties. For this reason, they are used in food supplements at high doses. The aim of this project was to determine the effects of kaempferol on oxidative stress and apoptosis in H4IIE rat hepatoma cells over a broad concentration range. Kaempferol is rapidly taken up and glucuronidated by H4IIE cells. The results demonstrate that kaempferol protects against H2O2-induced cellular damage at concentrations which lead to cell death and DNA strand breaks in the absence of H2O2-mediated oxidative stress. Preincubation with 50 microM kaempferol exerts protection against the loss of cell viability induced by 500 microM H2O2 (2 h) while the same concentration of kaempferol reduces cell viability by 50% in the absence of H2O2 (24 h). Preincubation with 50 microM kaempferol ameliorates the strong DNA damage induced by 500 microM H2O2 while 50 microM kaempferol leads to a significant increase of DNA breakage in the absence of H2O2. Preincubation with 50 microM kaempferol reduces H2O2-mediated caspase-3 activity by 40% (4 h) while the same concentration of kaempferol leads to the formation of a DNA ladder in the absence of H2O2 (24 h). It is concluded that the intake of high dose kaempferol in food supplements may not be advisable because in our cellular model protective kaempferol concentrations can also induce DNA damage and apoptosis by themselves.

Animals↗

PubMed2006

Enzymatic preparation of kaempferol from green tea seed and its antioxidant activity.

Among the flavonols in green tea, kaempferol has many biological activities but kaempferol of plant origin is too expensive to be used in commercial products. Recently, we confirmed that green tea seed (GTS) contained a reasonable amount of kaempferol glycoside. After conducting structure analysis, two kaempferol glycosides were identified, kaempferol-3-O-[2-O-beta-D-galactopyranosyl-6-O-alpha-L-rhamnopyranosyl]-beta-D-glucopyranoside (compound 1) and kaempferol-3-O-[2-O-beta-D-xylopyranosyl-6-O-alpha-L-rhamnopyranosyl]-beta-D-glucopyranoside (compound 2), respectively. Also, a commercially useful method for kaempferol preparation was suggested by enzymatic hydrolysis using these two flavonoids. After several enzyme reactions were performed for the complete bioconversion of compounds 1 and 2 to kaempferol, we found that the optimum enzyme combination was reaction with beta-galactosidase and hesperidinase. Finally, we produced pure kaempferol with over 95% purity. We also compared the antioxidant effect of these two GTS flavonoids and its aglycone, kaempferol. Kaempferol is a more efficient scavenger of 1,1-diphenyl-2-picrylhydrazyl radicals and a better inhibitor of xanthine/xanthine oxidase than the two glycosides.

Antioxidants↗

PubMed2003

Kaempferol-induced growth inhibition and apoptosis in A549 lung cancer cells is mediated by activation of MEK-MAPK.

A vast variety of naturally occurring substances have been shown to protect against experimental carcinogenesis and an increasing amount of evidence suggests that kaempferol may have cancer chemopreventative properties. However, the precise underlying protective mechanisms are poorly understood. To elucidate these mechanisms, we challenged human lung cancer cell line A549 with kaempferol and investigated its effects upon cellular growth and signal transduction pathways. Treatment of A549 cells with kaempferol resulted in a dose- and time-dependent reduction in cell viability and DNA synthesis with the rate of apoptosis equivalent to 0.9+/-0.5, 5.2+/-1.5, 16.8+/-2.0, 25.4+/-2.6, and 37.8+/-4.5% on treatment with 0, 17.5, 35.0, 52.5, and 70.0 microM kaempferol, respectively. Concomitantly, kaempferol treatments led to a 1.2-, 2.7-, 3.3-, and 3.4-fold increase in Bax. Similar elevations were also observed in Bad which increased 1.2-, 3.3-, 3.7-, and 4.7-fold, respectively, as compared to control. Bcl-2 and Bcl-xL expression were inhibited in a dose-dependent fashion. While the Akt-1 and phosphorylated Akt-1 were inhibited, the mitogen-activated protein kinase (MAPK) was activated upon kaempferol treatment. Kaempferol induced apoptosis was associated with the cleavage of caspase-7 and poly ADP-ribose polymerase (PARP). Inhibition of MEK1/2 but not PI-3 kinase blocked kaempferol-induced cleavage of caspase-7, PARP cleavage, and apoptosis. The results suggest that inactivation of Akt-1 and alteration of Bcl-2 family of proteins are not sufficient for kaempferol to induce apoptosis and activation of MEK-MAPK is a requirement for kaempferol-induced cell death machinery in A549 cells.

Antineoplastic Agents↗

PubMed1974

Kaempferol inhibitions of corn mitochondrial phosphorylation.

Kaempferol (3, 5, 7, 4'tetrahydroxyflavone) inhibited the rate of state 3 substrate oxidation, but not the state 4 rate. This, along with the kaempferol inhibition of substrate-driven calcium-phosphate deposition, provided evidence that kaempferol was acting specifically on the phosphorylation mechanism and not on electron transfer. Kaempferol, however, did not inhibit ATP-driven contraction while oligomycin did. Comparisons of kaempferol with mersalyl indicated that kaempferol did not inhibit phosphorylation by blocking phosphate transport. Both kaempferol and 2,4-dinitrophenol inhibited calcium-phosphate transport, but kaempferol did not stimulate respiration to the extent that 2,4-dinitrophenol did under acceptorless conditions. Kaempferol had no effect on NADH-driven contraction in a potassium chloride reaction medium. The site of kaempferol effect is thus seen to be unique from oligomycin and more like aurovertin, likely acting before the formation of the phosphorylated high energy intermediate, but not as an uncoupler in the traditional 2,4-dinitrophenol mode.

Journal Article↗

PubMed2006

Differential activity of kaempferol and quercetin in attenuating tumor necrosis factor receptor family signaling in bone cells.

Increasing data from epidemiological and in vitro studies show that the isoflavonoids, genistein and daidzein, and the flavonols, quercetin and kaempferol, are protective against postmenopausal bone loss. However, the physiological mechanisms for these effects are not well understood. We now report that kaempferol exerts profound antiosteoclastogenic effects by acting on both osteoblasts and osteoclasts. Kaempferol but not quercetin dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced production of the osteoclastogenic cytokines interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1/CCL2) in osteoblasts. The effect on IL-6 was posttranscriptional, whereas kaempferol reduced MCP-1 mRNA levels. In addition, in mouse primary calvarial osteoblasts, kaempferol but not quercetin blocked TNFalpha-induced translocation of the nuclear factor kappaB (NF-kappaB) subunit p65 from the cytoplasm to the nucleus. However, TNFalpha-stimulated intracellular ROS production was unaltered by kaempferol. In RAW264.7 cells, a monocyte/macrophage precursor for osteoclasts, both kaempferol and quercetin dose-dependently inhibited the receptor activator of NF-kappaB ligand (RANKL)-induced immediate-early oncogene c-fos expression at 6 h. After 3-5 days, both flavonols robustly inhibited RANKL-induced expression of the osteoclastic differentiation markers, RANK and calcitonin receptor. Consistent with down regulation of these osteoclastic differentiation markers, both flavonols strongly attenuated the RANKL-induced formation of multinucleated osteoclasts. However, kaempferol was more potent than quercetin in inhibiting RANKL-stimulated effects on RAW264.7 cells. Thus, our data indicate that kaempferol exerts profound antiosteoclastogenic effects by specifically antagonizing TNF receptor family action on bone cells at two distinct levels, by disrupting production of osteoclastogenic cytokines from osteoblasts and attenuating osteoclast precursor cell differentiation.

Animals↗

PubMed2004

Inhibition of estrogen receptor alpha expression and function in MCF-7 cells by kaempferol.

Estrogens are mitogenic for estrogen receptor (ER)-positive breast cancer cells. Current treatment of ER-positive breast tumors is directed towards interruption of estrogen activity. We report that treatment of ER-positive breast cancer cells with kaempferol resulted in a time- and dose-dependent decrease in cell number. The concentration required to produce 50% growth inhibition at 48 h was approximately 35.0 and 70.0 microM for ER-positive and ER-negative breast cancer cells, respectively. For MCF-7 cells, a reduction in the ER-alpha mRNA equivalent to 50, 12, 10% of controls was observed 24 h after treatment with 17.5, 35.0, and 70.0 microM of kaempferol, respectively. Concomitantly, these treatments led to a 58, 80, and 85% decrease in ER-alpha protein. The inhibitory effect of kaempferol on ER-alpha levels was seen as early as 6 h post-treatment. Kaempferol treatment also led in a dose-dependent decrease in the expression of progesterone receptor (PgR), cyclin D1, and insulin receptor substrate 1 (IRS-1). Immunocytochemical study revealed that ER-alpha protein in kaempferol-treated MCF-7 cells formed an aggregation in the nuclei. Kaempferol also induced degradation of ER-alpha by a different pathway than that were observed for the antiestrogen ICI 182,780 and estradiol. Estradiol-induced MCF-7 cell proliferation and expression of the estrogen-responsive-element-reporter gene activity were abolished in cells co-treated with kaempferol. These findings suggest that modulation of ER-alpha expression and function by kaempferol may be, in part, responsible for its anti-proliferative effects seen in in vitro.

Blotting, Northern↗

PubMed2006

Kaempferol enhances endothelium-independent and dependent relaxation in the porcine coronary artery.

The vascular effects of kaempferol were investigated in isolated porcine coronary artery rings. U46619 (9,11-dideoxy-9alpha, 11alpha-methanoepoxy prostaglandin F2alpha, 30 nM) was used to contract porcine coronary arterial rings. Concentration relaxation curve of kaempferol (1 nM - 100 microM) was constructed and kaempferol demonstrated significant relaxation at high concentrations. At low concentration with no significant effect on relaxation, kaempferol (10 microM) enhanced relaxation produced by bradykinin, the calcium ionophore A23187, isoproterenol and sodium nitroprusside in endothelium-intact porcine coronary arteries. In endothelium-disrupt rings, kaempferol (10 microM) also enhanced the relaxation caused by isoproterenol, sodium nitroprusside, levcromakalim and nifedipine. On the other hand, antioxidant agents did not affect bradykinin-induced relaxation or the enhancement effect of kaempferol. In summary, a low concentration of kaempferol (10 microM), devoid of significant vascular effect, has the ability to enhance endothelium-dependent and endothelium-independent relaxations. This action of kaempferol is unrelated to its antioxidant property.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2003

Potent inhibitory effect of naturally occurring flavonoids quercetin and kaempferol on in vitro osteoclastic bone resorption.

Several recent studies have suggested that flavonols, a class of phytochemicals with many biological activities, might exert a protective effect against post-menopausal bone loss. In the present study, we investigated the effects of quercetin and kaempferol, two of the major naturally occurring flavonols on the in vitro bone resorbing activity of osteoclasts. Our results indicate that both compounds, at concentrations ranging from 0.1 to 100 microM reduce bone resorption in a time and dose-dependent manner. Significant inhibitory effects were observed at concentrations as low as 0.1 microM especially with kaempferol. The IC(50)s, or concentration inhibitory of 50% of basal resorption, calculated for quercetin and kaempferol were 1.6 and 5.3 microM, respectively. Using highly purified rabbit osteoclasts, we showed that both flavonols directly induce apoptosis of mature osteoclasts in the same dose-range effective for inhibiting bone resorption. When osteoclasts were treated with 50 microM of quercetin and kaempferol, intracellular reactive oxygen species levels decreased significantly by 75 and 25%, respectively, indicating these molecules keep their antioxidant properties at this concentration. However, at concentrations below 50 microM, neither quercetin nor kaempferol exerted antiradical action, suggesting that antioxidant properties cannot fully explain the inhibitory effect on bone resorption. Finally, we report that kaempferol-, but not the quercetin-induced inhibition of bone resorption was partially abolished by the presence of the pure anti-estrogen ICI 182780 suggesting that kaempferol's estrogenic effect could be involved in the inhibition of bone resorption. The present study demonstrates that flavonols widely distributed in human diet such as quercetin and kaempferol, exert a potent inhibitory effect on in vitro bone resorption.

Animals↗

PubMed2003

Glucurono- and sulfo-conjugation of kaempferol in rat liver subcellular preparations and cultured hepatocytes.

Glucurono- and sulfo-conjugation of kaempferol in rat liver preparations and cultured hepatocytes were studied using high-performance liquid chromatography (HPLC) with two distinctly different elution solvents. Kaempferol glucuronides and sulfates were produced by treating kaempferol with microsomes plus UDPGA or with cytosol plus PAPS, respectively. HPLC analysis of the conjugates revealed one major and three minor glucuronides with solvent A and one sulfate with solvent B. Kaempferol metabolites produced by cultured hepatocytes also consisted of four glucuronides and one minor sulfate, all of which corresponded to their respective in vitro-produced conjugates in the liver subcellular preparations. The relative proportion of kaempferol sulfate accounted for about 9% of the total conjugates in the cultured hepatocytes. The kinetic data on glucurono- and sulfo-conjugation of kaempferol by the liver subcellular preparations correlated well with the preferential production of kaempferol glucuronides in the cultured hepatocytes. Glucurono- and sulfo-conjugation of 3-, 5- and 7-OH flavones in the liver subcellular preparations were also kinetically characterized. 7-OH flavone was predominantly conjugated to form a glucuronide compared to 3- and 5-OH flavones. These data suggest that glucuronidation at the 7-OH position on the A-ring is a major metabolic pathway of kaempferol in hepatic cells.

Animals↗

PubMed2006

The uptake behaviors of kaempferol and quercetin through rat primary cultured cortical neurons.

The objective of this study was to investigate whether kaempferol and quercetin could be transported into primary cultured cerebral neurons, to establish a practical HPLC method with UV detection for the two flavonols in the neurons, and to study the uptake and transport behaviors of them through the neurons. The present results showed that the level of kaempferol in the neurons increased linearly and then reached a plateau with incubation time at the high concentration of 10 microg/mL, but not at the other two concentrations of 1 and 0.1 microg/mL. However, the levels of quercetin in the neurons were not detected at the three incubating concentrations, and there was a new peak detected in the cell whose retention time was shorter (3.42 min) than that of quercetin (4.65 min). This phenomenon suggested that quercetin might be transported into the neurons and then metabolized quickly to some derivative. Kaempferol could be transported into the neurons in a concentration- and time-dependent manner when the neurons were incubated with the culture medium containing kaempferol at the high dose. There was an apparent correlation between the concentrations of kaempferol in the medium and in the cell, indicating that the uptake of kaempferol in the cell increased along with its dose (10 microg/mL). However, there was a negative correlation between the concentrations of quercetin in the medium and in the cell. The results suggested that kaempferol and quercetin were disposed by the neurons at different way, and this might be an important factor for their different effects on primary cultured cortical cells.

Animals↗

PubMed2002

The flavonoid Kaempferol suppresses the graft-versus-host reaction by inhibiting type 1 cytokine production and CD8+ T cell engraftment.

We have here examined the immunoregulatory effects of a natural flavonoid, Kaempferol, on T cells. Kaempferol suppressed IFN-gamma and IL-2 production but not that of IL-4 by T cells and shifted the Th1/Th2 balance into the Th2 phenotype. In C57BL/6 anti-BDF1 MLC, Kaempferol inhibited the development and expansion of type 1 effector CD8+ T cells and diminished allospecific CTL activity. Based on these in vitro results, we evaluated the effects of Kaempferol treatment on the development of C57BL/6-into-BDF1 acute graft-versus-host disease (GVHD). Brief administration of Kaempferol led to early recovery from body weight loss, increased survival, and reduced tissue injury in the liver and large intestine. Kaempferol treatment activated Th2 cells and the engraftment of donor cells and also diminished GVHD-associated antihost CTL activity. Thus, our study indicates that Kaempferol has the capacity to modulate the Th1/Th2 balance and could be useful for the treatment of cell-mediated immune diseases, such as acute GVHD.

Animals↗

PubMed2003

Determination of quercetin and kaempferol in human urine after orally administrated tablet of ginkgo biloba extract by HPLC.

A sensitive, simple and accurate method was developed for determination of quercetin and kaempferol in human urine by reversed phase high performance liquid chromatography. The urine samples were analyzed on C18 column. Quercetin and kaempferol were analyzed simultaneously with good separation. UV detector was set at 380 nm. There was a linear relationship between chromatographic area of analytes and concentration of analytes over the concentration range 1.638-81.90 and 1.872-93.60 ng/ml for quercetin and kaempferol, respectively. The recovery of the assay was 99.7+/-6.2 and 97.4+/-7.2% for quercetin and kaempferol, respectively. The within-day and between-day coefficients of variation were less than 9.7 and 16.5% (RSD), respectively. The limit of detection was 1.0 ng/ml for quercetin and 1.1 ng/ml for kaempferol. The limit of quantitation was 1.61+/-0.11 ng/ml (n=5) for quercetin and 1.85+/-0.11 ng/ml (n=5) for kaempferol. The method developed has been applied to determine quercetin and kaempferol after orally administrated tablet of Ginkgo biloba extract in human urine.

Calibration↗

PubMed2002

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.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗