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Antiartherosclerotic Effects of Plant Flavonoids

Shamala Salvamani, Baskaran Gunasekaran, Noor Azmi Shaharuddin and 2 more

BioMed Research International · 2014 · Review

doi:10.1155/2014/480258

Abstract

Atherosclerosis is the process of hardening and narrowing the arteries. Atherosclerosis is generally associated with cardiovascular diseases such as strokes, heart attacks, and peripheral vascular diseases. Since the usage of the synthetic drug, statins, leads to various side effects, the plants flavonoids with antiartherosclerotic activity gained much attention and were proven to reduce the risk of atherosclerosis in vitro and in vivo based on different animal models. The flavonoids compounds also exhibit lipid lowering effects and anti-inflammatory and antiatherogenic properties. The future development of flavonoids-based drugs is believed to provide significant effects on atherosclerosis and its related diseases. This paper discusses the antiatherosclerotic effects of selected plant flavonoids such as quercetin, kaempferol, myricetin, rutin, naringenin, catechin, fisetin, and gossypetin.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 25, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

Being a chronic inflammatory disease, atherosclerosis is becoming the leading cause of death in most of the developed countries. Cardiovascular diseases (CVDs) like myocardial infarction (heart attack), acute coronary syndrome, or stroke arise through the development of plaques and lesions inside the arteries. Hypercholesterolemia, hypertension, and obesity give high risks for the progression of CVDs. Statins are widely used as the clinical treatment for atherosclerosis due to its excellent efficacy in reducing the low density lipoprotein (LDL) level. Statins competitively inhibit the HMG-CoA reductase enzyme that plays a great role in catalyzing the rate-limiting step in the biosynthesis of cholesterol. The increase in hepatic LDL receptors' expression is triggered by the reduction of hepatocyte cholesterol concentration and helps to clear LDL from the circulation.

However, the consumption of statins causes adverse health effects such as liver injury and muscle toxicity. The other side effects include myopathy, rhabdomyolysis, and acute renal failure. Thus, attention is now directed to the natural products from plant origin that possess antiartherosclerotic activity and can promote human health. This can eventually avoid possible health effects due to the long period consumption of statins. Many researches on bioactive compounds and their possible medicinal attributes have been studied during the past decades. Plant and plant by-products can be used for isolating health-promoting bioactive compounds since there are substantial plant sources which are relatively inexpensive. The bioactive compound from plant extracts has shown plentiful health-promoting effects in both in vitro and in vivo studies, such as antioxidant, hypoglycemic, hypotensive, and hypocholesterolemic effects. The aim of this review is to provide the reader with some important evidence on the antiatherosclerotic activity of selected flavonoids that are mostly found in plants.

2. Flavonoids

Flavonoids represent a broad family of more than 4000 secondary plant metabolites. The four predominant classes are 4-oxoflavonoids (flavones and flavonols), isoflavones, anthocyanins, and flavan-3-ol derivatives (tannins and catechin). For centuries, preparations that contain flavonoids are applied as the primary physiologically active components that have been used for treating human diseases. Epidemiological studies have shown that the risk of heart diseases can be reduced through the consumption of flavonoid-rich diets. Flavonoids may inhibit the vascular diseases' development through alteration in endothelial cell eicosanoid production. Flavonoids also showed blood pressure lowering effect in hypertensive and normotensive subjects while flavonoids may have beneficial actions in obesity due to their capacity to regulate fatty oxidation and improve adipocyte functionality. Besides, food derived flavonols (quercetin, kaempferol, and myricetin) have been reported to exhibit various biological functions and medicinal properties such as antioxidant, antithrombotic, anti-inflammatory, anti atherogenic, antiatherosclerotic, and cardioprotective effects. The plants like Garcinia cambogia, Mangifera indica, Hypericum perforatum L, and Asparagus racemosus that contain flavonoids have been proven to significantly lower the risk of atherosclerosis and CVD.

2.1. Quercetin

Flavonoids such as quercetin (3′,4′,3,5,7-pentahydroxyflavone) have gained considerable attention mainly due to their broad spectrum of health beneficial effects for the treatment of CVDs. Quercetin has been reported to improve endothelium-dependent vasorelaxation in aorta, decreases systolic blood pressure, and reduces cardiac hypertrophy and proteinuria in hypertensive rats. Sánchez et al. reported that enhancement of endothelial nitric oxide synthase (eNOS) activity and reduction of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-mediated superoxide production with downregulation of p47phox expression showed the antihypertensive effects of quercetin. Besides that, quercetin has been proven to improve dyslipidemia, decrease oxidative stress through stimulation of lipolysis activity, and upregulate the adipocytes genes expression which increases the lipids beta oxidation. Quercetin treatment in obesity animal models showed reduction in body weight, visceral and subcutaneous adipose tissue, and liver fat accumulation. Moreover, quercetin also suppressed the peroxisome proliferator-activated receptor y (PPARy) and sterol regulatory element-binding proteins (SREBP) expression. The reduction in the expression of PPARy indicates reduction in adipogenesis. On the other hand, Morus alba L leaves containing quercetin 3-(6-malonylglucoside) (Q3MG) as their major flavonol attenuated the development of artherosclerotic lesion in LDL receptor-deficient mice through LDL resistance enhancement to oxidative modification and the artherosclerotic lesion in M. alba-treated mice was significantly reduced by 52%. Kleemann et al. reported on the anti-inflammatory and antiatherogenic effects of the quercetin and have shown that short-term treatment for 14 days with dietary quercetin managed to completely quench the cytokine-induced expression of human C-reactive protein (CRP) in transgenic mice. The elevating level of CRP is an inflammation marker that increases the risk of CVDs. Bhaskar et al. investigated the antiatherosclerotic property of quercetin and found notable regression of atherosclerosis in the histopathological examination of the aorta in hypercholesterolemic rabbits supplemented with quercetin. This suggests the potential of quercetin as an alternative therapeutic agent for atherosclerosis and CVDs as well as for hypertension and obesity that can lead to CVDs. Camellia chinensis, Allium fistulosum and Calamus scipionum, Moringa oleifera, Centella asiatica, Hypericum hircinum, and Hypericum perforatum have been reported to have high content of quercetin.

2.2. Kaempferol

Numerous researches have been conducted on kaempferol (3,4′,5,7-tetrahydroxyflavone) and studies have shown that consumption of kaempferol-rich foods reduced the risk of developing cardiovascular diseases. Kaempferol has been reported to increase endothelium relaxation in coronary artery of porcine. Xiao et al. investigated kaempferol's protective effects against endothelial damage and found that kaempferol improves the nitric acid production and reduces asymmetric dimethylarginine level which enhances the endothelium-dependent vasorelaxation, preventing endothelium injuries and oxidative damage in cells. The ability of kaempferol in reducing oxidative stress can be the beneficial effect in CDVs. Kaempferol also prevents arteriosclerosis by the inhibition of LDL oxidation and formation of platelets. Kowalski et al. demonstrated that the monocyte chemoattractant protein (MCP-1) is inhibited by kaempferol in an in vitro study. MCP-1 involves in the initial stage of plaque formation in arteriosclerosis. Kong et al. evaluated the effect of kaempferol on atherosclerosis induced rabbit models, and upon 10-week treatment of kaempferol with high cholesterol diet, the expression of intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and MCP-1 in the rabbits' aorta has been significantly downregulated. This indicates that kaempferol can alleviate vascular inflammation to prevent atherosclerosis. Moringa oleifera constitutes kaempferol as one of its major bioactive compound which was proven to possess antiatherosclerotic and hypolipidemic properties and has therapeutic potential in the treatment of hyperlipidemia, atherosclerosis, and cardiovascular diseases. Therefore, kaempferol can be considered to be an effective and potent agent against atherosclerosis. The presence of kaempferol has been identified in many other plants and some of them are Centella asiatica, Euonymus alatus, Kaempferia galanga L, Ginkgo biloba, Equisetum spp., Tilia spp., Sophora japonica, and propolis.

2.3. Myricetin

Myricetin (3,3′,4′,5,5′,7-hexahydroxyflavone) is a natural flavonol found in vegetables, fruits, berries, tea, and medicinal plants. Various health related studies on myricetin from plant sources have been demonstrated which revealed the antioxidant, antiviral, anticarcinogenic, antiplatelet, hypoglycemic, and cytoprotective properties of myricetin. Myricetin also possesses antihypertensive action. Godse et al. reported that myricetin prevent the progression of high blood pressure and reversed the metabolic alterations in fructose-induced rats. Besides, myricetin was proven to suppress body weight gain and fat accumulation by increasing oxidation of fatty acids which is due to upregulation of hepatic peroxisome proliferator activated receptor (PPARα) and downregulation of hepatic sterol regulatory element-binding proteins (SREBPs) expressions in high fat-induced rats. These results revealed the antiobesity and antihyperlipidemic effects of myricetin. Myricetin also was proven to possess protective effects on the oxidation of LDL in blood. Ha et al. reported that Ampelopsis cantoniensis has myricetin as its main constituent and managed to inhibit the LDL oxidation induced by metal ion (Cu2+) and free radical (AAPH), and therefore the A. cantoniensis extract can be utilized as a natural remedy to prevent the oxidation of LDL which is involved in the formation atherosclerotic lesion. Lian et al. revealed that besides preventing the LDL from oxidation, myricetin also blocks the oxidized LDL uptake by macrophages and plays an essential role in preventing atherosclerosis. In vivo studies on antiartherosclerotic effects of myricetin could further provide better knowledge and understanding of its role in ameliorating atherosclerosis. High content of myricetin has been also reported in these plants: Myrica cerifera L, Calamus scipionum, Chrysobalanus icaco L, Moringa oleifera, and Aloe vera.

2.4. Rutin

Rutin (quercetin-3-rutinoside) is a bioflavonoid commonly found in buckwheat bran, black tea, and citrus fruits. Rutin contributes to many positive health effects such as powerful antioxidant, protects against free radicals, possess anti-inflammatory properties, and suppresses aldose reductase activity. Endothelial dysfunction plays a major role in the development of CDVs and it is found in conditions such as hypertension, hypercholesterolemia, and atherosclerosis. Rutin in buckwheat extract decreases body weight, improves capillary fragility to maintain blood pressure, and significantly reduced nitrotyrosine immunoreactivity in endothelial cells of aorta. Rutin has been proven to exhibit antiobesity effect via suppression of oxidative stress, dyslipidemia, and hepatosteatosis in obese rats. Rutin decreases liver and adipose tissue weight, suppresses hepatic triacylglycerol and cholesterol level, and enhances antioxidant enzymes (superoxide dismutase and glutathione peroxidase) activities in obese rats. On the other hand, rutin plays a great role in preventing atherosclerosis and the evidence for its antiatherosclerotic effects is available in in vivo studies: rabbits, rat, and hamsters. Voskresensky and Bobyrev showed that rutin delays the hypercholesterolemia development and inhibits the atherosclerotic formation in rabbits' aorta. While, Santos et al. researched into the effects of rutin on controlling lipid metabolism and found that rutin reduced the cholesterol levels and has the lowest level of triacylglycerol in hypercholesterolemia rats. In addition, rutin extracted from Dimorphandra mollis showed decreases in the level of plasma triglyceride of hypercholesterolemia induced hamsters without changing the high-density lipoprotein (HDL) cholesterol and total cholesterol levels. Rutin was also proven to be nontoxic and no notable changes were observed in total white bloods cells and mononuclear and granulocytes cells compared to the untreated control group. Therefore, rutin can be developed as an alternative drug for the treatment of atherosclerosis. Other plants that constitute rutin compound are Flos hippocastani, Ruta graveolens, Rhus cotinus, and Phyllanthus amarus.

2.5. Naringenin

Naringenin (4′,5,7-trihydroxyflavanone) has been widely studied in issues related to atherosclerosis. Naringenin was reported to have poor antioxidant properties compared to other flavanoids but it is still able to be a potential inhibitor in cholesterol biosynthesis. Borradaile et al. claimed that naringenin regulates apolipoprotein B secretion by HepG2 cells directly through inhibition of cholesterol ester synthesis. Naringenin also reported to affect lipid metabolism through inhibition of acyl coenzyme A: cholesterol O-acyltransferase and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA) reductase in rats. Study on higher animal models, rabbits, was conducted by Kurowska et al. whereby the results obtained showed decrease in hepatic cholesterol and LDL levels. Meanwhile, studies performed on hypercholesterolemic human subjects showed increase in HDL levels after consumption of naringenin rich orange juices. Lee et al. demonstrated that (2S)-naringenin, isolated from Typha angustata, inhibits the vascular smooth muscle cells (VSMCs) proliferation while Mulvihill et al. reported that naringenin-treated mice showed about 60% reduction of aortic cholesterol and decreases the level of hepatic cholesteryl ester, very low-density lipoprotein (VLDL) and low density lipoprotein (LDL). These lead to the reduction in cholesterol and triglyceride accumulation within the arterial wall and ameliorates atherosclerosis. Besides, naringenin also prevents accumulation of adipose, adipocyte hypertrophy, and dyslipidemia. Other biological activities of naringenin include anti-inflammatory, anticancer, and positive effects on sex metabolism through binding to estrogen receptors. Naringenin is a potential flavonoid to be explored further especially in atherosclerosis since it has numerous health benefits. Some of the plant sources that are rich in naringenin are Solanum lycopersicum and citrus fruits, Mentha aquatica L, immature fruit of Citrus aurantium, and flowers of Acacia podalyriifolia.

2.6. Catechin

Catechin [(2R,3S)-3′,4′,5,7-tetrahydroxyflavan-3-ol] has been reported to effectively inhibit lipid peroxidation and scavenge free radicals. Catechin is known to possess preventive effect in CVDs due to its involvement in oxidative process in atherogenesis. Being antioxidant, catechin is able to modulate cellular signaling pathways that lead to elevation of vascular reactivity, platelet aggregation, and reduction of inflammation. Diverse studies have been conducted using tea (Camellia sinensis) which contains catechin believed to play a major role as cardioprotective plant source. Almost 50–80% of the total catechin from tea is epigallocatechin-3-gallate (EGCG) and it is considered to be the most effective bioactive component in cholesterol lowering. Proinflammatory cytokine and tumor necrosis factor-alpha (TNFα) commonly exist in atherosclerotic lesions which have direct effect on monocyte chemotactic protein-1 (MCP-1) stimulation and vascular endothelial cells. MCP-1 plays an important role in the monocytes' recruitment in developing inflammatory CDVs. EGCG inhibits TNFα activation and resulted in reduction of MCP-1 production in coronary vascular endothelial cell. Furuyashiki et al. demonstrated that EGCG at low concentration (5 μM) is able to suppress intracellular lipid accumulation in an in vitro model suggesting that the cholesterol lowering effect of EGCG is due to the influence on intestinal lipid absorption. Clinical studies done by Potenza et al. in hypertensive rats suggested that EGCG was shown to reduce blood pressure, raise adiponectin levels, protect against myocardial injury, and improve endothelial function which was proven to reduce the CVDs risk. Another study done by Bursill and Roach confirmed that EGCG lowers the cholesterol and triglyceride absorption in rats. Studies conducted on humans by Widlansky et al. claim that EGCG can reverse endothelial dysfunction and improve dilation of brachial artery in patients with coronary artery disease. These studies suggest the efficiency of EGCG as a potential agent for treating CVD. Other plant sources that are rich in catechins are Betula pubescens and Betula pendula, Cocos nucifera, fruit pulp of Argania spinosa, and Cassia fistula.

2.7. Fisetin

Fisetin (3,7,3′,4′-tetrahydroxyflavone) together with morin and myricetin is structural related flavan-3-ol and is commonly distributed in vegetables and fruits such as apple, strawberry, grape, persimmon, cucumber, and onion at concentrations of 2–160 μg/g. Fisetin is known for its strong antioxidative, anti-inflammatory, anticancer, antiproliferative, and antihyperglycemic activities. Increase in adipocyte cell number (hyperplasia) is an essential therapeutic target for the prevention of obesity. Jung et al. demonstrated that fisetin ameliorates diet-induced obesity by inhibition of mammalian target of rapamycin complex I (mTORCI) signalling which is central mediator for lipid biosynthesis, cellular growth, and proliferation. Fisetin supplementation in high-fat diet-induced mice regulated fat accumulation in adipose tissue and suppresses adipogenesis during the adipocyte differentiation via downregulation of related gene and thus the study proves that fisetin can be an effective antiobesity agent. The development of atherosclerotic lesion is induced by the elevated concentrations of LDL, blood cholesterol, and triglycerides. Macrophages play an essential role in the development of atherosclerosis by accumulating cholesterol in foam cells. Fisetin inhibits LDL oxidation by macrophages and plays a role as free radical scavenger in LDL which also inhibits the oxidative enzymes from macrophage. Thiobarbituric acid-reactive substances assay (TBARS), electrophoretic mobility, and conjugated diene formation analyses by Lian et al. have shown that fisetin inhibits Cu2+ mediated LDL oxidation stronger than morin and myricetin. Binding of CD36 (class B scavenger receptor) to oxidized LDL causes the formation of atherosclerotic lesion. Fisetin blocks macrophage's oxidized LDL uptake by reducing the CD36 expression on the macrophages. However, the study of fisetin in vivo atherosclerosis models is still lacking. The participation of fisetin in ameliorating atherosclerosis can further be confirmed in animal model studies for future flavonoids-based drugs. Plants like Butea frondosa, Gleditsia triacanthos, Quebracho colorado, Curcuma longa, Rhus verniciflua, Acacia greggii, and Acacia berlandieri are rich sources of fisetin.

2.8. Gossypetin

Gossypetin (3,5,7,8,3′,4′-hexahydroxyflavone) was originally isolated from Hibiscus spp.. Gossypetin suppressed the oxidation of LDL and was able to modify the LDL in a form accepted by macrophage through elevated affinity process in a nonoxidative mechanism. Lin et al. reported that gossypetin is an important flavonoid from Hibiscus sabdariffa and has been shown to prevent atherosclerosis, reduce oxidative stress, and neutralize agents that cause cancer. H. Sabdariffa extract revealed the potential of gossypetin in inhibiting atherosclerosis in hyperlipidemic rabbits. Chen et al. published the first report on the antiatherosclerotic activity of gossypetin in in vitro study and demonstrated that gossypetin inhibits both lipoprotein oxidation and lipid peroxidation. Gossypetin functions against oxidative LDL and accumulation of intracellular lipid through the regulation of peroxisome proliferator-activated receptor (PPAR) signals which stimulated the cholesterol to be removed from macrophages and retard the atherosclerosis process. The findings mentioned strongly suggest the development of gossypetin as an antiatherosclerotic agent. H. Sabdariffa extract has been used as antihypertensive agent since it decreases systolic blood and pulse pressure. Villalpando-Arteaga et al. reported that H. Sabdariffa aqueous extract possesses antilipidemic, antiobesity, and hepatoprotective effects. Studies on the role of gossypetin against hypertension and obesity can further reveal its beneficial effects and pharmacological activities. Besides H. Sabdariffa, gossypetin also is present in H. vitifolius, H. esculentus, Empetrum nigrum and Acacia constricta, H. rosa-sinensis, Chiranthodendron pentadactylon, Fremontia californica, Thespesia populnea, and Fagonia cretica.

3. Conclusion

The summary of reported plant flavonoids is shown in Table 1. Various flavonoids compounds that are available in plants exhibit numerous effects that can prevent the progression of atherosclerosis and diseases such as hypercholesterolemia, hypertension, and obesity that can lead to CVDs. In vivo studies on myricetin and fisetin could give better view on its potential as an antiatherosclerotic agent. Investigation of potential effects of gossypetin against hypertension and obesity is suggested. Future research can be focused on the role of plant flavonoids in human metabolism and signaling pathway involved during the therapy of atherosclerosis. This could help to determine the strategies of improving the alternatives therapeutic approaches for atherosclerosis and other related diseases. Since there is an urge for alternatives natural treatment due to the side effects of statins, flavonoid-based drugs can be utilized for the prevention and treatment of atherosclerosis and CVDs.

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  43. 43.

    Abbass A. Efficiency of some antioxidants in reducing cardio-metabolic risks in obese rats. Journal of American Science. 2011;7:1146-1159.

    Not in our library

  44. 44.

    Lee K-H, Park E, Lee H-J, et al. Effects of daily quercetin-rich supplementation on cardiometabolic risks in male smokers. Nutrition Research and Practice. 2011;5(1):28-33.

    Not in our library10.4162/nrp.2011.5.1.28

  45. 45.

    Stewart LK, Soileau JL, Ribnicky D, et al. Quercetin transiently increases energy expenditure but persistently decreases circulating markers of inflammation in C57BL/6J mice fed a high-fat diet. Metabolism: Clinical and Experimental. 2008;57(1):S39-S46.

    Not in our library10.1016/j.metabol.2008.03.003

  46. 46.

    Ohkoshi E, Miyazaki H, Shindo K, Watanabe H, Yoshida A, Yajima H. Constituents from the leaves of Nelumbo nucifera stimulate lipolysis in the white adipose tissue of mice. Planta Medica. 2007;73(12):1255-1259.

    Not in our library10.1055/s-2007-990223

  47. 47.

    Kobori M, Masumoto S, Akimoto Y, Oike H. Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western-style diet in C57/BL6J mice. Molecular Nutrition and Food Research. 2011;55(4):530-540.

    Not in our library10.1002/mnfr.201000392

  48. 48.

    Enkhmaa B, Shiwaku K, Katsube T, et al. Mulberry (Morus alba L.) leaves and their major flavonol quercetin 3-(6-malonylglucoside) attenuate atherosclerotic lesion development in LDL receptor-deficient mice. Journal of Nutrition. 2005;135(4):729-734.

    Not in our library10.1093/jn/135.4.729

  49. 49.

    Ridker PM. C-reactive protein: a simple test to help predict risk of heart attack and stroke. Circulation. 2003;108(12):e81-e85.

    Not in our library10.1161/01.cir.0000093381.57779.67

  50. 50.

    Bhaskar S, Kumar KS, Krishnan K, Antony H. Quercetin alleviates hypercholesterolemic diet induced inflammation during progression and regression of atherosclerosis in rabbits. Nutrition. 2013;29(1):219-229.

    Not in our library10.1016/j.nut.2012.01.019

  51. 51.

    Juźwiak S, Wójcicki J, Mokrzycki K, et al. Effect of quercetin on experimental hyperlipidemia and atherosclerosis in rabbits. Pharmacological Reports. 2005;57(5):604-609.

    Not in our library

  52. 52.

    Bhaskar S, Shalini V, Helen A. Quercetin regulates oxidized LDL induced inflammatory changes in human PBMCs by modulating the TLR-NF-κB signaling pathway. Immunobiology. 2011;216(3):367-373.

    Not in our library10.1016/j.imbio.2010.07.011

  53. 53.

    Hertog MGL, Hollman PCH, Van de Putte B. Content of potentially anticareinogenic flavonoids of tea infusions, wines, and fruit juices. Journal of Agricultural and Food Chemistry. 1993;41(8):1242-1246.

    Not in our library

  54. 54.

    Miean KH, Mohamed S. Flavonoid (myricetin, quercetin, kaempferol, luteolin, and apigenin) content of edible tropical plants. Journal of Agricultural and Food Chemistry. 2001;49(6):3106-3112.

    Not in our library10.1021/jf000892m

  55. 55.

    Siddhuraju P, Becker K. Antioxidant properties of various solvent extracts of total phenolic constituents from three different agroclimatic origins of drumstick tree (Moringa oleifera Lam.) leaves. Journal of Agricultural and Food Chemistry. 2003;51(8):2144-2155.

    Not in our library10.1021/jf020444+

  56. 56.

    Bajpai M, Pande A, Tewari SK, Prakash D. Phenolic contents and antioxidant activity of some food and medicinal plants. International Journal of Food Sciences and Nutrition. 2005;56(4):287-291.

    Not in our library10.1080/09637480500146606

  57. 57.

    Chimenti F, Cottiglia F, Bonsignore L, et al. Quercetin as the active principle of Hypericum hircinum exerts a selective inhibitory activity against MAO-A: extraction, biological analysis, and computational study. Journal of Natural Products. 2006;69(6):945-949.

    Not in our library10.1021/np060015w

  58. 58.

    Silva B, Oliveira PJ, Dias A, Malva JO. Quercetin, kaempferol and biapigenin from hypericum perforatum are neuroprotective against excitotoxic insults. Neurotoxicity Research. 2008;13(3-4):265-279.

    Not in our library10.1007/bf03033510

  59. 59.

    Knekt P, Kumpulainen J, Järvinen R, et al. Flavonoid intake and risk of chronic diseases. American Journal of Clinical Nutrition. 2002;76(3):560-568.

    Not in our library10.1093/ajcn/76.3.560

  60. 60.

    Calderon-Montano JM, Burgos-Morón E, López-Lázaro M. A review on the dietary flavonoid kaempferol. Mini Review in Medicinal Chemistry. 2011;11:298-344.

    Not in our library10.2174/138955711795305335

  61. 61.

    Xu YC, Yeung DKY, Man RYK, Leung SWS. Kaempferol enhances endothelium-independent and dependent relaxation in the porcine coronary artery. Molecular and Cellular Biochemistry. 2006;287(1-2):61-67.

    Not in our library10.1007/s11010-005-9061-y

  62. 62.

    Xiao H-B, Lu X-Y, Chen X-J, Sun Z-L. Protective effects of kaempferol against endothelial damage by an improvement in nitric oxide production and a decrease in asymmetric dimethylarginine level. European Journal of Pharmacology. 2009;616(1-3):213-222.

    Not in our library10.1016/j.ejphar.2009.06.022

  63. 63.

    Singh R, Singh B, Singh S, Kumar N, Kumar S, Arora S. Anti-free radical activities of kaempferol isolated from Acacia nilotica (L.) Willd. Ex. Del. Toxicology in Vitro. 2008;22(8):1965-1970.

    Not in our library10.1016/j.tiv.2008.08.007

  64. 64.

    Kowalski J, Samojedny A, Paul M, Pietsz G, Wilczok T. Effect of kaempferol on the production and gene expression of monocyte chemoattractant protein-1 in J774.2 macrophages. Pharmacological Reports. 2005;57(1):107-112.

    Not in our library

  65. 65.

    Kong L, Luo C, Li X, Zhou Y, He H. The anti-inflammatory effect of kaempferol on early atherosclerosis in high cholesterol fed rabbits. Lipids in Health and Disease. 2013;12(1):112-115.

    Not in our library10.1186/1476-511x-12-115

  66. 66.

    Chumark P, Khunawat P, Sanvarinda Y, et al. The in vitro and ex vivo antioxidant properties, hypolipidaemic and antiatherosclerotic activities of water extract of Moringa oleifera Lam. leaves. Journal of Ethnopharmacology. 2008;116(3):439-446.

    Not in our library10.1016/j.jep.2007.12.010

  67. 67.

    Rajanandh MG, Satishkumar MN, Elango K, Suresh B. Moringa oleifera Lam. A herbal medicine for hyperlipidemia: a pre-clinical report. Asian Pacific Journal of Tropical Disease. 2012;2(2):S790-S795.

    Not in our library

  68. 68.

    Fang X-K, Gao J, Zhu D-N. Kaempferol and quercetin isolated from Euonymus alatus improve glucose uptake of 3T3-L1 cells without adipogenesis activity. Life Sciences. 2008;82(11-12):615-622.

    Not in our library10.1016/j.lfs.2007.12.021

  69. 69.

    Sulaiman MR, Zakaria ZA, Daud IA, Ng FN, Ng YC, Hidayat MT. Antinociceptive and anti-inflammatory activities of the aqueous extract of Kaempferia galanga leaves in animal models. Journal of Natural Medicines. 2008;62(2):221-227.

    Not in our library10.1007/s11418-007-0210-3

  70. 70.

    Harnly JM, Doherty RF, Beecher GR, et al. Flavonoid content of U.S. fruits, vegetables, and nuts. Journal of Agricultural and Food Chemistry. 2006;54(26):9966-9977.

    Not in our library10.1021/jf061478a

  71. 71.

    Gray AM, Flatt PR. Nature’s own pharmacy: the diabetes perspective. Proceedings of the Nutrition Society. 1997;56(1999):507-517.

    Not in our library10.1079/pns19970051

  72. 72.

    Mira L, Fernandez MT, Santos M, Rocha R, Florêncio MH, Jennings KR. Interactions of flavonoids with iron and copper ions: a mechanism for their antioxidant activity. Free Radical Research. 2002;36(11):1199-1208.

    Not in our library10.1080/1071576021000016463

  73. 73.

    Cushnie TPT, Lamb AJ. Antimicrobial activity of flavonoids. International Journal of Antimicrobial Agents. 2005;26(5):343-356.

    Not in our library10.1016/j.ijantimicag.2005.09.002

  74. 74.

    Shimmyo Y, Kihara T, Akaike A, Niidome T, Sugimoto H. Three distinct neuroprotective functions of myricetin against glutamate-induced neuronal cell death: involvement of direct inhibition of caspase-3. Journal of Neuroscience Research. 2008;86(8):1836-1845.

    Not in our library10.1002/jnr.21629

  75. 75.

    Kang NJ, Jung SK, Lee KW, Lee HJ. Myricetin is a potent chemopreventive phytochemical in skin carcinogenesis. Annals of the New York Academy of Sciences. 2011;1229(1):124-132.

    Not in our library10.1111/j.1749-6632.2011.06122.x

  76. 76.

    Li Y, Ding Y. Minireview: therapeutic potential of myricetin in diabetes mellitus. Food Science and Human Wellness. 2012;1:19-25.

    Not in our library

  77. 77.

    Godse S, Mohan M, Kasture V, Kasture S. Effect of myricetin on blood pressure and metabolic alterations in fructose hypertensive rats. Pharmaceutical Biology. 2010;48(5):494-498.

    Not in our library10.3109/13880200903188526

  78. 78.

    Chang CJ, Tzeng T-F, Liou S-S, Chang Y-S, Liu I-M. Myricetin increases hepatic peroxisome proliferator-activated receptor protein expression and decreases plasma lipids and adiposity in rats. Evidence-Based Complementary and Alternative Medicine. 2012;2012:11 pages.

    Not in our library10.1155/2012/787152

  79. 79.

    Ha DT, Thuang PT, Thuan ND. Protective action of Ampelopsis cantoniensis and its major constituent—myricetin against LDL oxidation. Journal of Chemistry. 2007;45:768-771.

    Not in our library

  80. 80.

    Lian T-W, Wang L, Lo Y-H, Huang I-J, Wu M-J. Fisetin, morin and myricetin attenuate CD36 expression and oxLDL uptake in U937-derived macrophages. Biochimica et Biophysica Acta: Molecular and Cell Biology of Lipids. 2008;1781(10):601-609.

    Not in our library10.1016/j.bbalip.2008.06.009

  81. 81.

    Paul BD, Rao GS, Kapadia GJ. Isolation of myricadiol, myricitrin, taraxerol, and taraxerone from Myrica cerifera L. root bark. Journal of Pharmaceutical Sciences. 1974;63(6):958-959.

    Not in our library10.1002/jps.2600630638

  82. 82.

    Barbosa WLR, Peres A, Gallori S, et al. Determination of myricetin derivatives in Chrysobalanus icaco L., (Chrysobalanaceae). Brazilian Journal of Pharmacognosy. 2006;16:333-337.

    Not in our library

  83. 83.

    Kreft S, Knapp M, Kreft I. Extraction of rutin from buckwheat (Fagopyrum esculentum moench) seeds and determination by capillary electrophoresis. Journal of Agricultural and Food Chemistry. 1999;47(11):4649-4652.

    Not in our library10.1021/jf990186p

  84. 84.

    Metodiewa D, Kochman A, Karolczak S. Evidence for antiradical and antioxidant properties of four biologically active N,N-diethylamioethyl ethers of flavanone oximes: a comparison with natural polyphenolic flavonoid (rutin) action. International Union of Biochemistry and Molecular Life. 1997;41(5):1067-1075.

    Not in our library10.1080/15216549700202141

  85. 85.

    Aherne SA, O’Brien NM. Protection by the flavonoids myricetin, quercetin, and rutin against hydrogen peroxide-induced DNA damage in Caco-2 and Hep G2 cells. Nutrition and Cancer. 1999;34(2):160-166.

    Not in our library10.1207/s15327914nc3402_6

  86. 86.

    Guardia T, Rotelli AE, Juarez AO, Pelzer LE. Anti-inflammatory properties of plant flavonoids. Effects of rutin, quercetin and hesperidin on adjuvant arthritis in rat. Farmaco. 2001;56(9):683-687.

    Not in our library10.1016/s0014-827x(01)01111-9

  87. 87.

    Chan HJ, Ji YL, Chul HC, Chang JK. Anti-asthmatic action of quercetin and rutin in conscious guinea-pigs challenged with aerosolized ovalbumin. Archives of Pharmacal Research. 2007;30(12):1599-1607.

    Not in our library10.1007/bf02977330

  88. 88.

    Reddy GB, Muthenna P, Akileshwari C, Saraswat M, Petrash JM. Inhibition of aldose reductase and sorbitol accumulation by dietary rutin. Current Science. 2011;101(9):1191-1197.

    Not in our library

  89. 89.

    Dae WK, In KH, Soon SL, et al. Germinated buckwheat extract decreases blood pressure and nitrotyrosine immunoreactivity in aortic endothelial cells in spontaneously hypertensive rats. Phytotherapy Research. 2009;23(7):993-998.

    Not in our library10.1002/ptr.2739

  90. 90.

    Hsu C-L, Wu C-H, Huang S-L, Yen G-C. Phenolic compounds rutin and o-coumaric acid ameliorate obesity induced by high-fat diet in rats. Journal of Agricultural and Food Chemistry. 2009;57(2):425-431.

    Not in our library10.1021/jf802715t

  91. 91.

    Voskresensky ON, Bobyrev VN. Effect of ascorbic acid and rutin on the development of experimental peroxide atherosclerosis. Farmakologiyai Toksikologiya. 1979;42(4):378-382.

    Not in our library

  92. 92.

    Santos KFR, Oliveira TT, Nagem TJ, Pinto AS, Oliveira MGA. Hypolipidaemic effects of naringenin, rutin, nicotinic acid and their associations. Pharmacological Research. 1999;40(6):493-496.

    Not in our library10.1006/phrs.1999.0556

  93. 93.

    Kanashiro A, andrade DCO, Kabeya LM, et al. Modulatory effects of rutin on biochemical and hematological parameters in hypercholesterolemic Golden Syrian hamsters. Annals of the Brazilian Academy of Sciences. 2009;81(1):67-71.

    Not in our library10.1590/s0001-37652009000100009

  94. 94.

    Buszewski B, Kawka S, Suprynowicz Z, Wolski T. Simultaneous isolation of Rutin and Esculin from plant material and drugs using solid-phase extraction. Journal of Pharmaceutical and Biomedical Analysis. 1993;11(3):211-215.

    Not in our library10.1016/0731-7085(93)80199-b

  95. 95.

    Afshar DJ, Delazar A. Rutin from Ruta graveolens L. DARU Journal of Pharmaceutical Sciences. 1994;4:1-12.

    Not in our library

  96. 96.

    Atanassova M, Bagdassarian V. Rutin in plant products. Journal of the University of Chemical Technology and Metallurgy. 2009;44:201-203.

    Not in our library

  97. 97.

    Shukla P, Gopalkrishna B, Shukla P. Isolation of rutin from Phyllanthus amarus. International Journal of Pharmaceutical Sciences and Research. 2012;3:1198-1201.

    Not in our library

  98. 98.

    Jeon S-M, Bok S-H, Jang M-K, et al. Comparison of antioxidant effects of naringin and probucol in cholesterol-fed rabbits. Clinica Chimica Acta. 2002;317(1-2):181-190.

    Not in our library10.1016/s0009-8981(01)00778-1

  99. 99.

    Van Acker FAA, Schouten O, Haenen GRMM, Van Der Vijgh WJF, Bast A. Flavonoids can replace α-tocopherol as an antioxidant. FEBS Letters. 2000;473(2):145-148.

    Not in our library10.1016/s0014-5793(00)01517-9

  100. 100.

    Borradaile NM, Carroll KK, Kurowska EM. Regulation of HepG2 cell apolipoprotein B metabolism by the citrus flavanones hesperetin and naringenin. Lipids. 1999;34(6):591-598.

    Not in our library10.1007/s11745-999-0403-7

  101. 101.

    Lee S-H, Jeong T-S, Park YB, Kwon Y-K, Choi M-S, Bok S-H. Hypocholesterolemic effect of hesperetin mediated by inhibition of 3- hydroxy-3-methylgultaryl coenzyme A reductase and acyl coenzyme A: cholesterol acyltransferase in rats fed high-cholesterol diet. Nutrition Research. 1999;19(8):1245-1258.

    Not in our library

  102. 102.

    Lee SH, Park YB, Bae KH, et al. Cholesterol-lowering activity of naringenin via inhibition of 8-hydroxy-3-methylglutaryl coenzyme a reductase and acyl coenzyme A: cholesterol acyltransferase in rats. Annals of Nutrition and Metabolism. 1999;43(3):173-180.

    Not in our library10.1159/000012783

  103. 103.

    Kurowska EM, Borradaile NM, Spence JD, Carroll KK. Hypocholesterolemic effects of dietary citrus juices in rabbits. Nutrition Research. 2000;20(1):121-129.

    Not in our library

  104. 104.

    Kurowska EM, Spence JD, Jordan J, et al. HDL-cholesterol-raising effect of orange juice in subjects with hypercholesterolemia. American Journal of Clinical Nutrition. 2000;72(5):1095-1100.

    Not in our library10.1093/ajcn/72.5.1095

  105. 105.

    Lee J-J, Yi H, Kim I-S, et al. (2S)-Naringenin from Typha angustata inhibits vascular smooth muscle cell proliferation via a G0/G1 arrest. Journal of Ethnopharmacology. 2012;139:873-878.

    Not in our library10.1016/j.jep.2011.12.038

  106. 106.

    Mulvihill EE, Assini JM, Sutherland BG, et al. Naringenin decreases progression of atherosclerosis by improving dyslipidemia in high-fat-fed low-density lipoprotein receptor-null mice. Arteriosclerosis, Thrombosis, and Vascular Biology. 2010;30(4):742-748.

    Not in our library10.1161/atvbaha.109.201095

  107. 107.

    Ruh MF, Zacharewski T, Connor K, Howell J, Chen I, Safe S. Naringenin: a weakly estrogenic bioflavonoid that exhibits antiestrogenic activity. Biochemical Pharmacology. 1995;50(9):1485-1493.

    Not in our library10.1016/0006-2952(95)02061-6

  108. 108.

    Kuiper GGJM, Lemmen JG, Carlsson B, et al. Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor β. Endocrinology. 1998;139(10):4252-4263.

    Not in our library10.1210/endo.139.10.6216

  109. 109.

    Rosenberg RS, Grass L, Jenkins DJA, Kendall CWC, Diamandis EP. Modulation of androgen and progesterone receptors by phytochemicals in breast cancer cell lines. Biochemical and Biophysical Research Communications. 1998;248(3):935-939.

    Not in our library10.1006/bbrc.1998.8977

  110. 110.

    Déchaud H, Ravard C, Claustrat F, De La Perrière AB, Pugeat M. Xenoestrogen interaction with human sex hormone-binding globulin (hSHBG). Steroids. 1999;64(5):328-334.

    Not in our library10.1016/s0039-128x(98)00114-7

  111. 111.

    Manthey JA, Guthrie N, Grohmann K. Biological properties of citrus flavonoids pertaining to cancer and inflammation. Current Medicinal Chemistry. 2001;8(2):135-153.

    Not in our library10.2174/0929867013373723

  112. 112.

    Yoon K, Pallaroni L, Stoner M, Gaido K, Safe S. Differential activation of wild-type and variant forms of estrogen receptor α by synthetic and natural estrogenic compounds using a promoter containing three estrogen-responsive elements. Journal of Steroid Biochemistry and Molecular Biology. 2001;78(1):25-32.

    Not in our library10.1016/s0960-0760(01)00070-x

  113. 113.

    Krause M, Galensa R. Determination of naringenin and naringenin-chalcone in tomato skins by reversed phase HPLC after solid phase extraction. Zeitschrift für Lebensmittel-Untersuchung und -Forschung. 1992;194(1):29-32.

    Not in our library

  114. 114.

    Kawaii S, Tomono Y, Katase E, Ogawa K, Yano M. Quantitation of flavonoid constituents in Citrus fruits. Journal of Agricultural and Food Chemistry. 1999;47(9):3565-3571.

    Not in our library10.1021/jf990153+

  115. 115.

    Olsen HT, Stafford GI, van Staden J, Christensen SB, Jäger AK. Isolation of the MAO-inhibitor naringenin from Mentha aquatica L. Journal of Ethnopharmacology. 2008;117(3):500-502.

    Not in our library10.1016/j.jep.2008.02.015

  116. 116.

    Liu L, Shan S, Zhang K, Ning Z-Q, Lu X-P, Cheng Y-Y. Naringenin and hesperetin, two flavonoids derived from Citrus aurantium up-regulate transcription of adiponectin. Phytotherapy Research. 2008;22(10):1400-1403.

    Not in our library10.1002/ptr.2504

  117. 117.

    de Andrade CA, Carvalho JLDS, Cunico MM, et al. Antioxidant and antibacterial activity of extracts, fractions and isolated substances from the flowers of Acacia podalyriifolia A. Cunn. ex G. Don. Brazilian Journal of Pharmaceutical Sciences. 2010;46(4):715-721.

    Not in our library

  118. 118.

    Yoshino K, Hara Y, Sano M, Tomita I. Antioxidative effects of black tea theaflavins and thearubigin on lipid peroxidation of liver homogenates induced by tert-butyl hydroperoxide. Biological and Pharmaceutical Bulletin. 1994;17(1):146-149.

    Not in our library10.1248/bpb.17.146

  119. 119.

    Salah N, Miller NJ, Paganga G, Tijburg L, Bolwell GP, Rice-Evans C. Polyphenolic flavanols as scavengers of aqueous phase radicals and as chain-breaking antioxidants. Archives of Biochemistry and Biophysics. 1995;322(2):339-346.

    Not in our library10.1006/abbi.1995.1473

  120. 120.

    Gey KF. Ten-year retrospective on the antioxidant hypothesis of arteriosclerosis: threshold plasma levels of antioxidant micronutrients related to minimum cardiovascular risk. Journal of Nutritional Biochemistry. 1995;6(4):206-236.

    Not in our library

  121. 121.

    Vita JA. Tea consumption and cardiovascular disease: effects on endothelial function. Journal of Nutrition. 2003;133(10):3293s-3297s.

    Not in our library10.1093/jn/133.10.3293s

  122. 122.

    Stangl V, Lorenz M, Stangl K. The role of tea and tea flavonoids in cardiovascular health. Molecular Nutrition and Food Research. 2006;50(2):218-228.

    Not in our library10.1002/mnfr.200500118

  123. 123.

    Stangl V, Dreger H, Stangl K, Lorenz M. Molecular targets of tea polyphenols in the cardiovascular system. Cardiovascular Research. 2007;73(2):348-358.

    Not in our library10.1016/j.cardiores.2006.08.022

  124. 124.

    Shenouda SM, Vita JA. Effects of flavonoid-containing beverages and EGCG on endothelial function. Journal of the American College of Nutrition. 2007;26(4):366s-372s.

    Not in our library10.1080/07315724.2007.10719625

  125. 125.

    Khan N, Mukhtar H. Tea polyphenols for health promotion. Life Sciences. 2007;81(7):519-533.

    Not in our library10.1016/j.lfs.2007.06.011

  126. 126.

    Ahn HY, Xu Y, Davidge ST. Epigallocatechin-3-O-gallate inhibits TNFα-induced monocyte chemotactic protein-1 production from vascular endothelial cells. Life Sciences. 2008;82(17-18):964-968.

    Not in our library10.1016/j.lfs.2008.02.018

  127. 127.

    Furuyashiki T, Nagayasu H, Aoki Y, et al. Tea catechin suppresses adipocyte differentiation accompanied by down-regulation of PPARγ2 and C/EBPα in 3T3-L1 cells. Bioscience, Biotechnology and Biochemistry. 2004;68(11):2353-2359.

    Not in our library10.1271/bbb.68.2353

  128. 128.

    Potenza MA, Marasciulo FL, Tarquinio M, et al. EGCG, a green tea polyphenol, improves endothelial function and insulin sensitivity, reduces blood pressure, and protects against myocardial I/R injury in SHR. American Journal of Physiology: Endocrinology and Metabolism. 2007;292(5):E1378-E1387.

    Not in our library10.1152/ajpendo.00698.2006

  129. 129.

    Bursill CA, Roach PD. A green tea catechin extract upregulates the hepatic low-density lipoprotein receptor in rats. Lipids. 2007;42(7):621-627.

    Not in our library10.1007/s11745-007-3077-x

  130. 130.

    Widlansky ME, Hamburg NM, Anter E, et al. Acute EGCG supplementation reverses endothelial dysfunction in patients with coronary artery disease. Journal of the American College of Nutrition. 2007;26(2):95-102.

    Not in our library10.1080/07315724.2007.10719590

  131. 131.

    Ossipov V, Nurmi K, Loponen J, Haukioja E, Pihlaja K. High-performance liquid chromatographic separation and identification of phenolic compounds from leaves of Betula pubescens and Betula pendula. Journal of Chromatography A. 1996;721(1):59-68.

    Not in our library

  132. 132.

    Kirszberg C, Esquenazi D, Alviano CS, Rumjanek VM. The effect of a catechin-rich extract of Cocos nucifera on lymphocytes proliferation. Phytotherapy Research. 2003;17(9):1054-1058.

    Not in our library10.1002/ptr.1297

  133. 133.

    Charrouf Z, Guillaume D. Phenols and polyphenols from Argania spinosa. American Journal of Food Technology. 2007;2(7):679-683.

    Not in our library

  134. 134.

    Daisy P, Balasubramanian K, Rajalakshmi M, Eliza J, Selvaraj J. Insulin mimetic impact of Catechin isolated from Cassia fistula on the glucose oxidation and molecular mechanisms of glucose uptake on Streptozotocin-induced diabetic Wistar rats. Phytomedicine. 2010;17(1):28-36.

    Not in our library10.1016/j.phymed.2009.10.018

  135. 135.

    Arai Y, Watanabe S, Kimira M, Shimoi K, Mochizuki R, Kinae N. Dietary intakes of flavonols, flavones and isoflavones by Japanese women and the inverse correlation between quercetin intake and plasma LDL cholesterol concentration. Journal of Nutrition. 2000;130(9):2243-2250.

    Not in our library10.1093/jn/130.9.2243

  136. 136.

    Constantin RP, Constantin J, Pagadigorria CLS, et al. Prooxidant activity of fisetin: effects on energy metabolism in the rat liver. Journal of Biochemical and Molecular Toxicology. 2011;25(2):117-126.

    Not in our library10.1002/jbt.20367

  137. 137.

    Goh FY, Upton N, Guan S, et al. Fisetin, a bioactive flavonol, attenuates allergic airway inflammation through negative regulation of NF-κB. European Journal of Pharmacology. 2012;679(1-3):109-116.

    Not in our library10.1016/j.ejphar.2012.01.002

  138. 138.

    Yang P-M, Tseng H-H, Peng C-W, Chen W-S, Chiu S-J. Dietary flavonoid fisetin targets caspase-3-deficient human breast cancer MCF-7 cells by induction of caspase-7-associated apoptosis and inhibition of autophagy. International Journal of Oncology. 2012;40(2):469-478.

    Not in our library10.3892/ijo.2011.1203

  139. 139.

    Khan N, Afaq F, Syed DN, Mukhtar H. Fisetin, a novel dietary flavonoid, causes apoptosis and cell cycle arrest in human prostate cancer LNCaP cells. Carcinogenesis. 2008;29(5):1049-1056.

    Not in our library10.1093/carcin/bgn078

  140. 140.

    Prasath GS, Subramanian SP. Modulatory effects of fisetin, a bioflavonoid, on hyperglycemia by attenuating the key enzymes of carbohydrate metabolism in hepatic and renal tissues in streptozotocin-induced diabetic rats. European Journal of Pharmacology. 2011;668(3):492-496.

    Not in our library10.1016/j.ejphar.2011.07.021

  141. 141.

    Lee Y, Bae EJ. Inhibition of mitotic clonal expansion mediates fisetin-exerted prevention of adipocyte differentiation in 3T3-L1 cells. Archives of Pharmacal Research. 2013;36:1377-1384.

    Not in our library10.1007/s12272-013-0226-z

  142. 142.

    Jung CH, Kim H, Ahn J, Jeon T-I, Lee D-H, Ha T-Y. Fisetin regulates obesity by targeting mTORC1 signaling. The Journal of Nutritional Biochemistry. 2013;24(8):1547-1554.

    Not in our library10.1016/j.jnutbio.2013.01.003

  143. 143.

    Reed J. Cranberry flavonoids, atherosclerosis and cardiovascular health. Critical Reviews in Food Science and Nutrition. 2002;42(3):301-316.

    Not in our library10.1080/10408390209351919

  144. 144.

    Steinberg D, Parthasarathy S, Carew TE, Khoo JC, Witztum JL. Beyond cholesterol: modifications of low-density lipoprotein that increase its atherogenicity. The New England Journal of Medicine. 1989;320(14):915-924.

    Not in our library10.1056/nejm198904063201407

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    De Whalley CV, Rankin SM, Hoult JRS, Jessup W, Leake DS. Flavonoids inhibit the oxidative modification of low density lipoproteins by macrophages. Biochemical Pharmacology. 1990;39(11):1743-1750.

    Not in our library10.1016/0006-2952(90)90120-a

  146. 146.

    Gábor M, Eperjessy E. Antibacterial effect of fisetin and fisetinidin. Nature. 1966;212(5067):p. 1273.

    Not in our library10.1038/2121273a0

  147. 147.

    Lako J, Trenerry VC, Wahlqvist M, Wattanapenpaiboon N, Sotheeswaran S, Premier R. Phytochemical flavonols, carotenoids and the antioxidant properties of a wide selection of Fijian fruit, vegetables and other readily available foods. Food Chemistry. 2007;101(4):1727-1741.

    Not in our library

  148. 148.

    Lee J-D, Huh J-E, Jeon G, et al. Flavonol-rich RVHxR from Rhus verniciflua stokes and its major compound fisetin inhibits inflammation-related cytokines and angiogenic factor in rheumatoid arthritic fibroblast-like synovial cells and in vivo models. International Immunopharmacology. 2009;9(3):268-276.

    Not in our library10.1016/j.intimp.2008.11.005

  149. 149.

    Forbes TDA, Clement BA. Chemistry of Acacia's from South Texas. Texas A&M Agricultural Research and Extension Center. 2010;4-14.

    Not in our library

  150. 150.

    Lin H-H, Chen J-H, Wang C-J. Chemopreventive properties and molecular mechanisms of the bioactive compounds in Hibiscus sabdariffa linne. Current Medicinal Chemistry. 2011;18(8):1245-1254.

    Not in our library10.2174/092986711795029663

  151. 151.

    Chen JH, Tsai CW, Wang CP, Lin HH. Anti-atherosclerotic potential of gossypetin via inhibiting LDL oxidation and foam cell formation. Toxicology and Applied Pharmacology. 2013;272:313-324.

    Not in our library10.1016/j.taap.2013.06.027

  152. 152.

    Harborne JB. Gossypetin and herbacetin as taxonomic markers in higher plants. Phytochemistry. 1969;8(1):177-183.

    Not in our library

  153. 153.

    Bendz G. Chemistry in Botanical Classification: Medicine and Natural Sciences. 2013.

    Not in our library

  154. 154.

    Rankin SM, De Whalley CV, Hoult JRS, et al. The modification of low density lipoprotein by the flavonoids myricetin and gossypetin. Biochemical Pharmacology. 1993;45(1):67-75.

    Not in our library10.1016/0006-2952(93)90378-a

  155. 155.

    Mozaffari-Khosravi H, Jalali-Khanabadi B-A, Afkhami-Ardekani M, Fatehi F, Noori-Shadkam M. The effects of sour tea (Hibiscus sabdariffa) on hypertension in patients with type II diabetes. Journal of Human Hypertension. 2009;23(1):48-54.

    Not in our library10.1038/jhh.2008.100

  156. 156.

    Villalpando-Arteaga EV, Mendieta-Condado E, Esquivel-Solís H, et al. Hibiscus sabdariffa L. aqueous extract attenuates hepatic steatosis through down-regulation of PPAR-γ and SREBP-1c in diet-induced obese mice. Food & Function. 2013;4:618-626.

    Not in our library10.1039/c3fo30270a

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