Dietary soy protein isolate ameliorates atherosclerotic lesions in apolipoprotein E-deficient mice potentially by inhibiting monocyte chemoattractant protein-1 expression

Soy-based diets reportedly protect against the development of atherosclerosis; however, the underlying mechanism(s) for this protection remains unknown. In this report, the mechanism(s) contributing to the atheroprotective effects of a soy-based diet was addressed using the apolipoprotein E knockout (apoE-/-) mice fed soy protein isolate (SPI) associated with or without phytochemicals (SPI+ and SPI-, respectively) or casein (CAS). Reduced atherosclerotic lesions were observed in aortic sinus and enface analyses of the descending aorta in SPI+- or SPI(-)-fed apoE-/- mice compared with CAS-fed mice. SPI+-fed mice showed 20% fewer lesions compared with SPI(-)-fed mice. Plasma lipid profiles did not differ among the 3 groups, suggesting alternative mechanism(s) could have contributed to the atheroprotective effect of soy-based diets. Real-time quantitative PCR analyses of proximal aorta showed reduced expression of monocyte chemoattractant protein-1 (MCP-1), a monocyte chemokine, in mice fed both soy-based diets compared with the CAS-fed mice. These findings paralleled the reduced number of macrophages observed in the lesion site in the aorta of SPI+- or SPI(-)-fed mice compared with CAS-fed mice. In an in vitro LPS-induced inflammation model, soy isoflavones (genistein, daidzein, and equol alone or in combination) dose dependently inhibited LPS-induced MCP-1 secretion by macrophages, suggesting a role for soy isoflavones for the protective in vivo effects. Collectively, these findings suggest that the reduction in atherosclerotic lesions observed in mice fed the soy-based diet is mediated in part by inhibition of MCP-1 that could result in reduced monocyte migration, an early event during atherogenesis.     

Soy protein reduces paraquat-induced oxidative stress in rats

The effect of soy protein, soy isoflavones and saponins on paraquat (PQ)-induced oxidative stress was investigated in rats. Rats were fed experimental diets containing casein (CAS), soy protein (SPI), and casein with soy isoflavones and saponins (CAS + IS). The diets were supplemented or not with 0.025% paraquat (CAS + PQ, SPI + PQ, and CAS + IS + PQ). The protective effects of soy protein, soy isoflavones, and saponins on paraquat-induced oxidative stress were examined. Ingestion of soy protein generally mitigated the lung enlargement (P = 0.076), loss of body weight (P = 0.051) and oxidation of liver lipid (P = 0.043) and glutathione (P = 0.035) induced by paraquat, although soy isoflavones and saponins did not. To determine whether soy protein exerted its antioxidative effects by preventing paraquat absorption from digestive organs, rats were fed CAS or SPI diets and orally administered a 12.5 g/L paraquat solution. Plasma, urine, and fecal paraquat concentrations did not differ between the two groups, indicating that soy protein did not prevent paraquat absorption. The present study suggests that intake of soy protein itself, but not soy isoflavones and saponins, reduces paraquat-induced oxidative stress in rats, although this effect was not due to reduced absorption of paraquat from digestive organs.     

Dietary soy isoflavones and estrone protect ovariectomized ERalphaKO and wild-type mice from carcinogen-induced colon cancer

Consumption of soy foods has been weakly associated with reduced colon cancer risk. Colon cancer risk is influenced by estrogen exposure, although the mechanism through which this occurs is not defined. Conversion of estradiol (E2) to estrone (E1) may be protective in the colon. We hypothesized that dietary phytoestrogens, or E1, would reduce colon tumorigenesis via an estrogen receptor (ER)-dependent mechanism. Ovariectomized ERalphaKO or wild-type (WT) female mice were fed diets containing casein (Casein), soy protein without isoflavones (Soy-IF), soy protein + genistein (Soy+Gen), soy protein + NovaSoy (Soy+NSoy) or soy protein + estrone (Soy+E1) from weaning. Colon tumors were induced with azoxymethane. Tumor incidence was affected by diet but not genotype. Colon tumor incidence was lower in ERalphaKO and WT mice fed the Soy+E1 diet compared with those fed the casein or Soy-IF diets. Mice fed Soy+NSoy had a lower tumor incidence than mice fed casein, but not Soy-IF. Genistein did not affect tumor incidence. Soy protein, independently of phytoestrogens or E1, significantly reduced relative colon weight, tumor burden and multiplicity. Relative colon weight was lower (P=0.008) in mice fed Soy+E1 than in the other soy-fed groups. Tumor incidence in this group was lower than in the casein and soy-IF-fed groups and tended to be lower than in the others (P=0.020). Hence, soy protein and NSoy protect mice from colon cancer, and E1 further reduces colon tumorigenesis in mice, independently of ERalpha.     

Bone mass and soy isoflavones in socially housed, premenopausal macaques

BACKGROUND: Soy consumption is associated with a lower incidence of hip fracture in Asian than in Western women, an effect often attributed to estrogen-like compounds (isoflavones) in soy. It is not known whether premenopausal soy exposure initiated in adulthood can increase bone mass and thereby reduce fracture risk. OBJECTIVE: We aimed to determine whether a high-isoflavone soy diet influences bone mass in soy-na?ve, premenopausal cynomolgus monkeys (Macaca fascicularis). DESIGN: Ninety-four skeletally mature females were randomly assigned to consume diets whose protein content came from either high-isoflavone soy or casein and lactalbumin. Animals were socially housed. Bone mass and circulating isoflavone concentrations were measured at baseline and 19 and 31 mo after the start of treatment; bone biomarkers were measured at baseline and 31 mo. RESULTS: There were no significant differences at any timepoint in whole-body bone mineral content between casein-fed (112.5 +/- 2.1, 119.2 +/- 1.9, and 120.7 +/- 2.1 g) and soy-fed (117.2 +/- 2.1, 122.4 +/- 2.0, and 125.4 +/- 2.3 g; P=0.12) monkeys. Similar results were seen for spinal bone mineral density (casein-fed: 0.46 +/- 0.01, 0.50 +/- 0.01, and 0.52 +/- 0.01 g/cm(2); soy-fed: 0.47 +/- 0.01, 0.51 +/- 0.01, and 0.52 +/- 0.01 g/cm(2); P=0.30) and bone biomarker measurements-bone-specific alkaline phosphatase (soy-fed: 82.3 +/- 4.1 and 63.2 +/- 3.4 ng/mL; casein-fed: 94.1 +/- 4.5 and 61.7 +/- 4.3 ng/mL; P=0.22) and C-terminal crosslink of type 1 collagen (soy-fed: 0.944 +/- 0.06 and 0.89 +/- 0.08 nmol/L; casein-fed: 0.97 +/- 0.07 and 0.78 +/- 0.06 nmol/L; P=0.20). CONCLUSION: A soy diet high in isoflavones does not significantly affect bone characteristics in initially soy-na?ve premenopausal monkeys.     

Nutritional and antinutritional aspects of an Argentinian soy flour assessed on weanling rats

Inactivation of antinutritional factors on an Argentinian deffated soy flour was evaluated in relation to its corresponding original soybeans. Residual urease and trypsin inhibitors activities, protein solubility, available lysine and phytic acid showed acceptable levels. The nutritional value of a diet based on the same soy flour was compared with that of a casein-based diet by allowing them to each one of two groups of weanling IIMBeta rats during 28 days. Non-significant differences were obtained between groups comparing both body weight gain per gram of protein intake as well as the results of histometric studies performed on the small intestine. Thus, this soy flour contained appropriately inactivated antinutritional factors and its protein content and quality were nutritionally suitable. Large intestine hypertrophy was revealed within the soy-fed group suggesting increased microbial proliferation attributable to non-digestible oligosaccharides and fiber-like compounds. These compounds, employed by gut microflora as fermentation substrates, would be also responsible for an increased nitrogen excretion in the soy-fed group in relation to controls. This increment of nitrogen excretion significantly lowered the value of apparent nitrogen digestibility in the soy-fed group in relation to the casein-fed control one. Nevertheless, nitrogen apparent digestibility in the soy-fed group was equal or higher than other values reported from distinct treated soy meal-based diets.     

Inducibility of hepatic CYP1A enzymes by 3-methylcholanthrene and isosafrole differs in male rats fed diets containing casein, soy protein isolate or whey from conception to adulthood

Hepatic cytochrome P450 (CYP)1A1 and 1A2 enzymes were studied in male Sprague-Dawley rats derived from 5-7 litters fed diets in which the protein source was casein, soy protein isolate or whey. At age 65 d, rats were gavaged with corn oil (vehicle), 40 mg/kg 3-methylcholanthrene (3-MC) or 75 mg/kg isosafrole (ISO). Hepatic expression of CYP1A1 and CYP1A2 mRNA, apoprotein and associated monooxygenase activities were measured 17 h later. No significant dietary effects were observed on basal expression of either enzyme. However, interactions between diet and the two inducers (3-MC and ISO) were observed in soy-fed rats for ethoxy- and methoxyresorufin O-dealkylase activity, CYP1A1 and CYP1A2 apoprotein and mRNA (P < 0.05). The level of induction of CYP1A1 mRNA and apoprotein was lower in rats fed soy diets than in rats fed casein diets (P < 0.05), and the level of induced CYP1A2 mRNA was lower in rats fed soy or whey (P < 0.05) after treatment with the aryl hydrocarbon (Ah) receptor-dependent inducer 3-MC. This was accompanied by a 50% reduction in constitutive levels of the Ah receptor in liver cytosol of soy-fed, relative to casein-fed rats, and a slightly smaller reduction in whey-fed rats. Expression of the Ah receptor correlated with 3-MC-inducibility of CYP1A1 mRNA in rats fed the three diets. In contrast, in rats induced with ISO, which does not bind to the Ah receptor and induces CYP1As via different mechanisms than 3-MC, ethoxyresorufin O-deethylase activity and levels of CYP1A1 apoprotein and mRNA were elevated to a greater degree in soy-fed than in casein- or whey-fed rats (P < 0.05). Moreover, after ISO treatment, induction of methoxyresorufin O-demethylase activity, CYP1A2 apoprotein and mRNA levels was observed only in rats fed soy (P < 0.05). These data suggest potential effects of dietary protein source on metabolism of a wide variety of CYP1A substrates, including environmental and dietary carcinogens, many of which induce their own metabolism.     

Moderate-intensity, premeal cycling blunts postprandial increases in monocyte cell surface CD18 and CD11a and endothelial microparticles following a high-fat meal in young adults

High-fat meals promote transient increases in proatherogenic factors, implicating the postprandial state in cardiovascular disease (CVD) progression. Although low-grade inflammation is associated with CVD, little research has assessed postprandial inflammation. Because of its anti-inflammatory properties, premeal exercise may counteract postprandial inflammation. The purpose of this study was to determine postprandial alterations in monocytes and circulating markers of endothelial stress and inflammation following a high-fat meal in young adults with or without premeal cycle exercise. Each subject completed two trials and was randomized to rest or cycle at a moderate intensity prior to eating a high-fat meal. Flow cytometry was used to assess monocyte cell surface receptor expression and concentration of endothelial microparticles (EMP). Plasma cytokines were assessed using Luminex MagPix. Statistical analysis was completed using separate linear mixed models analyses with first-order autoregressive (AR(1)) heterogeneous covariance structure. Significance was set at P?≤ 0.05. Percentage increases in classic monocyte CD11a and CD18 were greater overall in the postprandial period in the meal-only condition compared with the meal?+ exercise condition (P?< 0.05). EMP concentration was 47% greater 3 h after the meal compared with premeal values in the meal-only condition (P?< 0.05); no significant increase was observed in the meal?+ exercise condition. Premeal cycling blunted postprandial increases in EMP and CD11a and CD18. Acute, moderate-intensity exercise may help counteract possibly deleterious postprandial monocyte and endothelial cell activation.     

Genistein prevents hyperglycemia-induced monocyte adhesion to human aortic endothelial cells through preservation of the cAMP signaling pathway and ameliorates vascular inflammation in obese diabetic mice

Hyperglycemia-induced vascular inflammation resulting in the enhanced monocyte-endothelial cell (EC) interaction is the key event in the pathogenesis of atherosclerosis in diabetes. Here, we investigated the effect of isoflavone genistein on hyperglycemia-stimulated vascular inflammation. Human aortic EC (HAEC) were pretreated with genistein before the addition of high glucose (HG; 25 mmol/L) for 48 h. Genistein at a physiological concentration (0.1 μmol/L) significantly inhibited HG-induced adhesion of monocytes to HAEC and suppressed endothelial production of monocyte chemotactic protein-1 (MCP-1) and IL-8. Inhibition of adenylate cyclase or protein kinase A (PKA) significantly attenuated the antiadhesion effect of genistein. Consistently, genistein improved HG-impaired intracellular cAMP production and PKA activity in HAEC. Six-week-old diabetic db/db mice were untreated (db/db) or treated with a diet containing 1 g genistein/kg diet (db/db+G) for 8 wk. Their nondiabetic db/+ mice were used as normal controls. Circulating concentrations of MCP-1/JE and KC were significantly greater, whereas IL-10 concentrations were lower in db/db mice than those in normal mice. Dietary supplementation of genistein did not normalize but significantly suppressed the elevated serum concentrations of MCP-1/JE from 286 ± 30 ng/L to 181 ± 35 ng/L and KC from 321 ± 21 ng/L to 232 ± 20 ng/L while increasing that of IL-10 from 35 ± 4 ng/L to 346 ± 35 ng/L in db/db+G mice. Further, genistein treatment suppressed diabetes-induced adhesion of monocytes to EC by 87% and endothelial secretion of adhesion molecules. We conclude that genistein improves diabetes-caused vascular inflammation, which may be mediated through promoting the cAMP/PKA pathway.     

Plasma, tissue and fecal cholesterol of young pigs fed restricted or liberal amounts of beef, soy or conventional diets

Cholesterol disposition (tissue deposition + fecal excretion) was determined in young pigs fed restricted (trial 1) or liberal (trial 2) amounts of beef-based, soy-based or conventional swine diets. Cholesterol content of diet is greater than average United States consumption per kilogram body weight but is very similar on a per-kilocalorie intake basis. Both beef and soy diets contained more cholesterol (0.09% by weight vs. 0%) and fat (40-50% of calories vs. 8-9%) than did conventional diets. Dried egg yolk was the source of cholesterol in the soy diets. Beef- and soy-fed pigs had greater plasma, HDL and LDL cholesterol concentrations than did conventionally fed pigs; beef-fed pigs had greater plasma, HDL and LDL cholesterol concentrations than did soy-fed pigs in trial 2 only. Final HDL-to-LDL cholesterol ratios did not differ. Neutral steroid and bile acid excretion was twofold greater in soy-fed than in conventionally or beef-fed pigs in trial 2 only. Differences in cholesterol concentrations were found in liver (soy, beef greater than conventional) and heart (soy greater than beef, conventional) in trial 1 and in liver (soy, beef greater than conventional), adipose tissue (soy greater than conventional greater than beef) and aorta and other viscera (conventional greater than soy, beef) in trial 2. In both trials, soy-fed pigs had greatest whole-body cholesterol concentrations. Thus, in both trials, disposition of cholesterol was similar in conventionally fed and beef-fed pigs, despite greater cholesterol intake in the latter, but was greater soy-fed pigs.     

Soy isoflavones improve spatial delayed matching-to-place performance and reduce cholinergic neuron loss in elderly male rats

To investigate the protective activity of soy isoflavones on neurons, the effects of isoflavones on cholinergic enzyme activity, immunoreactivities of cholinergic enzyme, and delayed matching-to-place (DMP) performance were measured in normal elderly rats. Male Sprague-Dawley rats (n = 48; 10 mo old) were assigned to 3 groups: CD (control diet), ISO 0.3 (0.3 g/kg soy isoflavones diet), and ISO 1.2 (1.2 g/kg soy isoflavones diet). After 16 wk of consuming these diets, choline acetyltransferase (ChAT) activity in the ISO 0.3 group was greater in cortex and basal forebrain (BF; P < 0.05) than in controls. In BF, ChAT activity was also significantly greater in the ISO 1.2 group than in control rats. Acetylcholine esterase (AChE) activity in the ISO 0.3 group was significantly inhibited in cortex, BF, and hippocampus and in the ISO 1.2 group in cortex and hippocampus. Choline acetyltransferase immunoreactivity (ChAT-IR) in the ISO 1.2 group was significantly greater than in controls in the medial septum area. ChAT-IR in the ISO 0.3 and ISO 1.2 groups was significantly higher than in the CD group in the hippocampus CA1 area. Spatial DMP performance by the ISO 0.3 group showed significantly shorter swimming time than by the CD group. These findings show that soy isoflavones can influence the brain cholinergic system and reduce age-related neuron loss and cognition decline in male rats.     

Resveratrol blunts tumor necrosis factor-��-induced monocyte adhesion and transmigration

The leukocyte recruitment and transmigration across the endothelial barrier into the vessel wall are crucial steps in atherosclerosis. Leukocyte trafficking on the endothelium is elicited by induction of endothelial adhesion molecules, and its transmigration is mediated by degradation of basement membrane proteins through enzymatic activity of matrix metalloproteinases (MMP). The current study investigated whether resveratrol, a polyphenol present in grapes and red wine, was capable of inhibiting leukocyte adhesion to tumor necrosis factor (TNF)-α-activated endothelium. It was found that resveratrol inhibited the TNF-α-activated endothelial expression of vascular cell adhesion molecule-1 in a dose-dependent manner. In addition, resveratrol hampered THP-1 monocyte adhesion to activated endothelial cells. This study further examined whether resveratrol interfered with transendothelial migration of leukocytes. The MMP-2 gelatinolytic activity of endothelial cells was enhanced by TNF-α, which was attenuated by an addition of ≥25 µM resveratrol. In addition, 25 µM resveratrol mitigated the MMP-9 activity of THP-1 cells, followed by a marked inhibition of transendothelial migration. These results demonstrated that resveratrol suppressed monocyte adhesion and migration induced by TNF-α through modulating expression of adhesion molecules and gelatinolytic activity of MMP. These findings suggest that dietary resveratrol may be therapeutic agent for inhibiting leukocyte recruitment into the subendothelium during inflammatory atherosclerosis.     

Dietary soy protein isolate and isoflavones modulate hepatic thyroid hormone receptors in rats

Thyroid hormone receptors (TRs) are regulators of many genes involved in cholesterol and lipid metabolism. The purpose of this study was to examine the effect of soy protein isolate (SPI) and isoflavones on hepatic TRs in rats. In Expt. 1, Sprague-Dawley rats were fed diets containing either casein or alcohol-washed SPI with or without isoflavone supplementation (5-1250 mg/kg diet) for 70, 190, and 310 d. The offspring (F1) were fed the same diets as their parents (F0). In Expt. 2, Sprague-Dawley rats were fed diets containing casein or casein plus isoflavones (50-400 mg/kg diet) for 120 d. The mRNA and protein contents of the hepatic TRs were measured by semiquantitative RT-PCR and Western blot, respectively. TRalpha1, TRalpha2, and TRbeta2 contents were not affected by SPI. However, the content of the 52-kDa TRbeta1 protein, the major isoform present in the liver, was markedly increased by dietary SPI in both sexes of F0 and F1 compared with casein. The supplemental isoflavones had no effect on TRbeta1, whereas the high doses of isoflavones (250 and 1250 mg/kg diet) reduced the hepatic TRalpha1 protein content in F1 male rats on d 28. SPI had no effect on total T3 and T4 levels. However, higher dose of supplemental isoflavones markedly increased T4 level in female rats. Overall, this study demonstrates for the first time that SPI upregulates hepatic TRbeta1 expression, and that isoflavones reduce the hepatic TRalpha1 level in young male rats. The SPI-induced TRbeta1 may play a role in mediating the hypocholesterolemic and lipid-lowering actions of soy protein.     

Regulation of male sex hormone levels by soy isoflavones in rats

Several studies have suggested that soybean intake is associated with a lower risk of prostate cancer. However, the mechanism of prostate cancer prevention by soybeans remains unclear. Because prostate cancer is reported to have an association with an increased level of dihydrotestosterone (DHT) and soybean isoflavones are known to inhibit 5 alpha-reductase, which is involved in the conversion of testosterone to DHT, the effects of soybean extract and isoflavones on the plasma levels of male sex hormones were investigated using male rats. In Experiment I, Sprague-Dawley rats were fed diets with and without soy flour; in Experiment II, rats were fed diets containing 2% soy methanol extract or 0.2% semipurified isoflavones or a control diet. The study showed a reduction of plasma DHT along with an increase in total plasma androgen in rats fed soy flour or semipurified isoflavones for 1 wk. These results suggest that soy isoflavone intake may reduce plasma DHT level.     

A cooperative interaction between soy protein and its isoflavone-enriched fraction lowers hepatic lipids in male obese Zucker rats and reduces blood platelet sensitivity in male Sprague-Dawley rats

Soy protein diets lower plasma cholesterol in hyperlipoproteinemic human subjects, as well as in animal models. We fed 7-wk-old male obese (fa/fa) and lean Zucker rats a modified AIN-76 diet (20 g protein/kg diet) containing casein (C), low isoflavone soy protein (38 mg isoflavones/kg diet; LI), or high isoflavone soy protein (578 mg isoflavones/kg diet; HI) for 70 d. In obese rats, plasma total cholesterol was 21 and 29% lower in the LI and HI groups, respectively, than in the C group (P: 相似文献   

Anti-inflammatory effects of isoflavones are dependent on flow and human endothelial cell PPARgamma

The mechanisms by which isoflavones protect against inflammatory vascular disease remain unclear. Our previous observations suggest that one mechanism involves inhibition of monocyte-endothelial cell interactions in a process that is absolutely dependent on flow. The molecular mechanisms involved and the effects of structurally distinct isoflavones on this process are not known and are investigated herein. Using static and flow-dependent monocyte adhesion assays, our data show that exposure of endothelial cells to biologically relevant concentrations of isoflavones inhibits subsequent TNF-alpha induced monocyte adhesion only during flow. This inhibition involved activating endothelial PPARgamma by stimulating promoter sequences containing the PPARgamma response element by isoflavones and attenuating antiadhesive effects by siRNA targeting of PPARgamma. A comparison of structurally distinct isoflavones suggested a critical role for the A-ring. Using chlorinated derivatives of daidzein, a key structural requirement for PPARgamma agonist activity appears to be the presence of the 7-OH group and the lack of chlorine at the 6- or 8-positions in the A-ring. Collectively, these data support 1) a novel flow-dependent anti-inflammatory mechanism for PPARgamma ligands in vascular endothelial cells and 2) exemplify the current concepts of nutrients modulating disease via regulating specific cell signaling pathways.     

Fructooligosaccharide and soy isoflavone suppress colonic aberrant crypt foci and cyclooxygenase-2 expression in dimethylhydrazine-treated rats

This study investigated the inhibitory effects of soy isoflavones and fructooligosaccharide (FOS) on colon carcinogenesis. Sprague-Dawley male rats were injected with 1,2-dimethylhydrazine (DMH) and given experimental diets that contained 0%, 3%, 6%, or 9% FOS with or without soy isoflavones (1,000 mg/kg of diet). After 12 weeks, colonic aberrant crypt foci (ACF) formation, cyclooxygenase-2 (COX-2) expression, and fecal bile acid profiles were determined. The numbers of ACF, the numbers of ACF containing four or more crypts per focus of colonic mucosa, and the levels of COX-2 protein in the colonic epithelial tissues were significantly decreased in a dose-dependent manner in the FOS-fed, DMH-treated rats (P < .001), as compared to the DMH-treated control rats. Soy isoflavones significantly decreased the number of ACF with four or more aberrant crypts per focus (P < .001) and the amount of COX-2 protein (P < .01), independently of the effect of the oligosaccharide. The highest suppression of ACF formation was obtained with soy isoflavones combined with >or=6% FOS. No significant relationship was found between the dosage of FOS or soy isoflavones and the concentration of fecal secondary bile acid. We conclude that the combination of FOS and soy isoflavones inhibits colonic ACF formation and reduces COX-2 expression in DMH-treated rats.     

Effect of genistein and daidzein on platelet aggregation and monocyte and endothelial function

There has been much recent interest in the cardiovascular benefits of dietary isoflavones. The aim of the present in vitro studies was to investigate potential anti-thrombogenic and anti-atherogenic effects of the isoflavones genistein and daidzein in platelets, macrophages and endothelial cells. Pre-treatment with either isoflavone inhibited collagen-induced platelet aggregation in a dose-dependent manner. In a macrophage cell line (RAW 264.7) activated with interferon gamma plus lipopolysaccharide, both isoflavones were found to inhibit NO production and tumour necrosis factor alpha (TNF-alpha) secretion dose-dependently, but they did not affect mRNA levels for inducible nitric oxide synthase and cyclo-oxygenase-2. Both isoflavones also dose-dependently decreased monocyte chemoattractant protein-1 secretion induced by TNF-alpha in human umbilical vein endothelial cells. Compared with daidzein, genistein exerted greater inhibitory effects for all parameters studied. The present data contributes to our knowledge on the molecular mechanisms by which isoflavones may protect against coronary artery disease. Further studies are required to determine whether the effects of isoflavones observed in the current in vitro studies are relevant to the aetiology of coronary artery disease in vivo.