Dietary Polyphenols-Important Non-Nutrients in the Prevention of Chronic Noncommunicable Diseases. A Systematic Review

Wojciech Koch, Wojciech Koch

Abstract

The improvement of the social and economic conditions of society has eliminated the threat of death from the majority of infectious diseases. However, the rapid progress of civilization has created new possibilities for the appearance of factors with adverse effects for the health of society. This has led to increased morbidity from certain diseases, the presence of which had not been observed several centuries ago. Chronic noncommunicable diseases (e.g., cancers, cardio-vascular disorders, diabetes, obesity, neurodegenerative diseases) result from an inappropriate relationship between people and their environment. The common characteristic for all chronic diseases is a "new" form of inflammation, very often called metaflammation, which is considered as a subclinical, permanent inflammation. As a result, metabolic cascade, including cellular oxidative stress, atherosclerotic process, and insulin resistance, occurs, which slowly generates significant deterioration in the organism. Polyphenols are the major group of non-nutrients, considering their diversity, food occurrence, and biological properties. The current review aims to present a wide spectrum of literature data, including the molecular mechanism of their activity and experimental model used, and summarize the recent findings on the multitude of physiological effects of dietary polyphenols towards the prevention of several chronic diseases. However, despite several studies, the estimation of their dietary intake is troublesome and inconclusive, which will be also discussed.

Keywords: chronic noncommunicable diseases; dietary intake; flavonoids; polyphenols.

Figures

Figure 1
Figure 1
The most common methods used to estimate dietary intake of polyphenols.
Figure 2
Figure 2
Biological properties of dietary polyphenols important in lifestyle diseases prevention.

References

    1. Carrera-Bastos P., Fontes-Villalba M., O’Keefe J.H., Lindeberg S., Cordain L. The western diet and lifestyle and diseases of civilization. Res. Rep. Clin. Cardiol. 2011;2:15–35. doi: 10.2147/RRCC.S16919.
    1. Betlejewski S. Social diseases, civilization diseases or lifestyle diseases? Wiad. Lek. 2007;60:489–492.
    1. Cordain L., Eaton S.B., Sebastian A., Mann N., Lindeberg S., Watkins B.A., O’Keefe J.H., Brand-Miller J. Origins and evolution of the Western diet: Health implications for the 21st century. Am. J. Clin. Nutr. 2005;81:341–354. doi: 10.1093/ajcn.81.2.341.
    1. Booth F.W., Lees S.J. Fundamental questions about genes, inactivity, and chronic diseases. Physiol. Genom. 2007;28:146–157. doi: 10.1152/physiolgenomics.00174.2006.
    1. Egger G., Dixon J. Beyond obesity and lifestyle: A review of 21st century chronic diseases determinants. BioMed Res. Int. 2014;2014:731685. doi: 10.1155/2014/731685.
    1. Lindeberg S. Food and Western Disease: Health and Nutrition from an Evolutionary Perspective. Wiley-Blackwell; Chichester, UK: 2010.
    1. Eaton S.B., Konner M., Shostak M. Stone agers in the fast lane: Chronic degenerative diseases in evolutionary perspective. Am. J. Med. 1988;84:739–749. doi: 10.1016/0002-9343(88)90113-1.
    1. Jönsson T., Olsson S., Ahrén B., Bøg-Hansen T.C., Dole A., Lindeberg S. Agrarian diet and diseases of affluence: Do evolutionary novel dietary lectins cause leptin resistance? BMC Endocr. Disord. 2005;5:10. doi: 10.1186/1472-6823-5-10.
    1. Cordain L. Implications of Plio-Pleistocene hominin diets for modern humans. In: Ungar P., editor. Evolution of the Human Diet: The Known, the Unknown, and the Unknowable. Oxford University Press; New York, NY, USA: 2007. pp. 363–383.
    1. Cordain L. Cereal grains: Humanity’s double-edged sword. World Rev. Nutr. Diet. 1999;84:19–73.
    1. Chaplin G., Jablonski N.G. Vitamin D and the evolution of human depigmentation. Am. J. Phys. Anthropol. 2009;139:451–461. doi: 10.1002/ajpa.21079.
    1. Vieth R. What is the optimal vitamin D status for health? Prog. Biophys. Mol. Biol. 2006;92:26–32. doi: 10.1016/j.pbiomolbio.2006.02.003.
    1. Deutch B., Dyerberg J., Pedersen H.S., Aschlund E., Hansen J.C. Traditional and modern Greenlandic food: Dietary composition, nutrients and contaminants. Sci. Total Environ. 2007;384:106–119. doi: 10.1016/j.scitotenv.2007.05.042.
    1. Kuhnlein H.V., Receveur O. Local cultural animal food contributes high levels of nutrients for Arctic Canadian indigenous adults and children. J. Nutr. 2007;137:1110–1114. doi: 10.1093/jn/137.4.1110.
    1. Wiley T.S., Formby B. Lights Out: Sleep, Sugar and Survival. Pocket Books; New York, NY, USA: 2000.
    1. Rook G.A. 99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: Darwinian medicine and the ‘hygiene’ or ‘old friends’ hypothesis. Clin. Exp. Immunol. 2010;160:70–79. doi: 10.1111/j.1365-2249.2010.04133.x.
    1. Booth F.W., Chakravarthy M.V., Gordon S.E., Spangenburg E.E. Waging war on physical inactivity: Using modern molecular ammunition against an ancient enemy. J. Appl. Physiol. 2002;93:3–30. doi: 10.1152/japplphysiol.00073.2002.
    1. Pettee K.K., Ainsworth B.E. The Building Healthy Lifestyles Conference: Modifying lifestyles to enhance physical activity, diet, and reduce cardiovascular disease. Am. J. Lifestyle Med. 2009;3:6–10. doi: 10.1177/1559827609336385.
    1. Cordain L., Gotshall R.W., Eaton S.B., Eaton S.B., 3rd Physical activity, energy expenditure and fitness: An evolutionary perspective. Int. J. Sports Med. 1998;19:328–335. doi: 10.1055/s-2007-971926.
    1. Eaton S.B. The ancestral human diet: What was it and should it be a paradigm for contemporary nutrition? Proc. Nutr. Soc. 2006;65:1–6. doi: 10.1079/PNS2005471.
    1. Fox L.C., Juan J., Albert R.M. Phytolith analysis on dental calculus, enamel surface, and burial soil: Information about diet and paleoenviroment. Am. J. Phys. Anthropol. 1996;101:101–113. doi: 10.1002/(SICI)1096-8644(199609)101:1<101::AID-AJPA7>;2-Y.
    1. Cordain L., Brand Miller J., Eaton S.B., Mann N., Holt S.H.A., Speth J.D. Plant to animal subsistence ratios and macronutrient energy estimations in worldwide huntergatherer diets. Am. J. Clin. Nutr. 2000;71:682–692. doi: 10.1093/ajcn/71.3.682.
    1. Kuipers R.S., Luxwolda M.F., Janneke Dijck-Brouwer D.A., Eaton S.B., Crawford M.A., Cordain L., Muskiet F.A. Estimated macronutrient and fatty acid intakes from an East African Paleolithic diet. Br. J. Nutr. 2010;104:1666–1687. doi: 10.1017/S0007114510002679.
    1. McKeown T. The Origins of Human Disease. Basil Blackwell; New York, NY, USA: 1998.
    1. Sanders J.W., Fuhrer G.S., Johnson M.D., Riddle M.S. The epidemiological transition: The current status of infectious diseases in the developed world versus the developing world. Sci. Prog. 2008;91:1–38. doi: 10.3184/003685008X284628.
    1. Hotamisligil G.S. Inflammation and metabolic disorders. Nature. 2006;444:860–867. doi: 10.1038/nature05485.
    1. Hotamisligil G.S., Shargill N.S., Spiegelman B.M. Adipose expression of tumor necrosis factor-α: Direct role in obesity-linked insulin resistance. Science. 1993;259:87–91. doi: 10.1126/science.7678183.
    1. Medzhitov R. Origin and physiological roles of inflammation. Nature. 2008;454:428–435. doi: 10.1038/nature07201.
    1. Libby P. Inflammatory mechanisms: The molecular basis of inflammation and disease. Nutr. Rev. 2007;65:140–146. doi: 10.1301/nr.2007.dec.S140-S146.
    1. Gregor M.F., Hotamisligil G.S. Inflammatory mechanisms in obesity. Ann. Rev. Immunol. 2011;29:415–445. doi: 10.1146/annurev-immunol-031210-101322.
    1. Hanson G.K. Inflammation, atherosclerosis and coronary artery disease. N. Engl. J. Med. 2005;352:1658–1695. doi: 10.1056/NEJMra043430.
    1. Egger G., Dixon J. Inflammatory effects of nutritional stimuli: Further support for the need for a big picture approach to tackling obesity and chronic disease. Obes. Rev. 2010;11:137–149. doi: 10.1111/j.1467-789X.2009.00644.x.
    1. Egger G., Dixon J. Non-nutrient causes of low-grade, systemic inflammation: Support for a “canary in the mineshaft” view of obesity in chronic disease. Obes. Rev. 2011;12:339–345. doi: 10.1111/j.1467-789X.2010.00795.x.
    1. Egger G. In search of a “germ theory” equivalent for chronic Disease. Prev. Chronic Dis. 2012;9:1–7. doi: 10.5888/pcd9.110301.
    1. Black P.H. The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X. Brain Behav. Immun. 2003;17:350–364. doi: 10.1016/S0889-1591(03)00048-5.
    1. Mills N.L., Donaldson K., Hadoke P.W., Boon N.A., MacNee W., Cassee F.R., Sandström T., Blomberg A., Newby D.E. Adverse cardiovascular effects of air pollution. Nat. Clin. Pract. Cardiovasc. Med. 2009;6:36–44. doi: 10.1038/ncpcardio1399.
    1. Vardavas C.I., Panagiotakos D.B. The causal relationship between passive smoking and inflammation on the development of cardiovascular disease: A review of the evidence. Inflamm. Allergy Drug Targets. 2009;8:328–333. doi: 10.2174/1871528110908050328.
    1. Tilg H., Moschen A.R. Inflammatory mechanisms in the regulation of insulin resistance. Mol. Med. 2008;14:222–231. doi: 10.2119/2007-00119.Tilg.
    1. Kolb H., Mandrup-Poulsen T. The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation. Diabetologia. 2010;53:10–20. doi: 10.1007/s00125-009-1573-7.
    1. Tasali E., Leproult R., Spiegel K. Reduced sleep duration or quality: Relationships with insulin resistance and type 2 diabetes. Prog. Cardiovasc. Dis. 2009;51:381–391. doi: 10.1016/j.pcad.2008.10.002.
    1. Krueger P.M., Friedman E.M. Sleep duration in the United States: A cross-sectional population-based study. Am. J. Epidemiol. 2009;169:1052–1063. doi: 10.1093/aje/kwp023.
    1. Holick M.F. Vitamin D deficiency. N. Engl. J. Med. 2007;357:266–281. doi: 10.1056/NEJMra070553.
    1. World Health Organization . Diet, Nutrition, and the Prevention of Chronic Diseases. WHO; Geneva, Switzerland: 2003.
    1. Nicholas L., Roberts D., Pond D. The role of the general practitioner and the dietitian in patient nutrition management. Asia Pac. J. Clin. Nutr. 2003;12:3–8.
    1. Australian Institute of Health and Welfare, Chronic Diseases. [(accessed on 3 March 2018)]; Available online: .
    1. Galland L. Diet and inflammation. Nutr. Clin. Pract. 2010;25:634–664. doi: 10.1177/0884533610385703.
    1. Barbaresko J., Koch M., Schulze M.B., Nothlings U. Dietary pattern analysis and biomarkers of low-grade inflammation: A systematic literature review. Nutr. Rev. 2013;71:511–527. doi: 10.1111/nure.12035.
    1. O’Neil C.E., Keast D.R., Fulgoni V.L., Nicklas T.A. Food sources of energy and nutrients among adults in the US: NHANES 2003-2006. Nutrients. 2012;4:2097–2120. doi: 10.3390/nu4122097.
    1. Cordain L., Eades M.R., Eades M.D. Hyperinsulinemic diseases of civilization: More than just Syndrome X. Comp. Biochem. Physiol. A Mol. Integr. Physiol. 2003;136:95–112. doi: 10.1016/S1095-6433(03)00011-4.
    1. Barclay A.W., Petocz P., McMillan-Price J., Flood V.M., Prvan T., Mitchell T., Brand-Miller J.C. Glycemic index, glycemic load, and chronic disease risk: A meta-analysis of observational studies. Am. J. Clin. Nutr. 2008;87:627–637. doi: 10.1093/ajcn/87.3.627.
    1. Alas-Salvadó J., Farrés X., Luque X., Narejos S., Borrel M., Basora J., Anguera A., Torres F., Bullo M., Balanza R. Effect of two doses of a mixture of soluble fibres on body weight and metabolic variables in overweight or obese patients: A randomised trial. Br. J. Nutr. 2008;99:1380–1387. doi: 10.1017/S0007114507868528.
    1. Tarini J., Wolever T.M. The fermentable fibre inulin increases postprandial serum short-chain fatty acids and reduces free fatty acids and ghrelin in healthy subjects. Appl. Physiol. Nutr. Metab. 2010;35:9–16. doi: 10.1139/H09-119.
    1. National Health and Nutrition Examination Survey. [(accessed on 7 April 2018)]; Available online: .
    1. Danaei G., Ding E.L., Mozaffarian D., Taylor B., Rehm J., Murray C.J., Ezzati M. The preventable causes of death in the United States: Comparative risk assessment of dietary, lifestyle, and metabolic risk factors. PLoS Med. 2009;6:e1000058. doi: 10.1371/journal.pmed.1000058.
    1. Xiao Y., Zhang Y., Wang M., Li X., Xia M., Ling W. Dietary protein and plasma total homocysteine, cysteine concentrations in coronary angiographic subjects. Nutr. J. 2013;12:144. doi: 10.1186/1475-2891-12-144.
    1. Miller D.B., O’Callaghan J.P. Biomarkers of Parkinson’s disease: Present and future. Metabolism. 2015;64:40–46. doi: 10.1016/j.metabol.2014.10.030.
    1. Ceriello A., Motz E. Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited. Arterioscler. Thromb. Vasc. Biol. 2004;24:816–823. doi: 10.1161/01.ATV.0000122852.22604.78.
    1. De la Monte S.M., Neely T.R., Cannon J. Oxidative stress and hypoxia, molecular abnormalities in central nervous system neurons. Cell. Mol. Life Sci. 2000;57:1471–1481. doi: 10.1007/PL00000630.
    1. Robertson R.P., Harmon J., Tran P.O., Tanaka Y., Takahashi H. Glucose toxicity in-cells: Type 2 diabetes, good radicals gone bad, and the glutathione connection. Diabetes. 2003;52:581–587. doi: 10.2337/diabetes.52.3.581.
    1. Paolisso G., Giugliano D. Oxidative stress and insulin action. Is there a relationship? Diabetologia. 1996;39:357–363. doi: 10.1007/BF00418354.
    1. Kinkade K., Streeter J., Miller F.J., Jr. Inhibition of NADPH oxidase by apocynin attenuates progression of atherosclerosis. Int. J. Mol. Sci. 2013;14:17017–17028. doi: 10.3390/ijms140817017.
    1. Sugiyama S., Kugiyama K., Aikawa M., Nakamura S., Ogawa H., Libby P. Hypochlorous acid, a macrophage product, induces endothelial apoptosis and tissue factor expression: Involvement of myeloperoxidase-mediated oxidant in plaque erosion and thrombogenesis. Arterioscler. Thromb. Vasc. Biol. 2004;24:1309–1314. doi: 10.1161/01.ATV.0000131784.50633.4f.
    1. Csanyi G., Yao M., Rodriguez A.I., Al Ghouleh I., Sharifi-Sanjani M., Frazziano G., Huang X., Kelley E.E., Isenberg J.S., Pagano P.J. Thrombospondin-1 regulates blood flow via CD47 receptor-mediated activation of NADPH oxidase 1. Arterioscler. Thromb. Vasc. Biol. 2012;32:2966–2973. doi: 10.1161/ATVBAHA.112.300031.
    1. Touyz R.M., Briones A.M. Reactive oxygen species and vascular biology: Implications in human hypertension. Hypertens. Res. 2011;34:5–14. doi: 10.1038/hr.2010.201.
    1. Heitzer T., Schlinzig T., Krohn K., Meinertz T., Münzel T. Endothelial dysfunction, oxidative stress, and risk of cardiovascular events in patients with coronary artery disease. Circulation. 2001;104:2673–2678. doi: 10.1161/hc4601.099485.
    1. Koch W., Baj T., Kukula-Koch W., Marzec Z. Dietary intake of specific phenolic compounds and their effect on the antioxidant activity of daily food rations. Open Chem. 2015;13:869–876. doi: 10.1515/chem-2015-0100.
    1. Huxley R.R., Neil H.A. The relation between dietary flavonol intake and coronary heart disease mortality: A meta-analysis of prospective cohort studies. Eur. J. Clin. Nutr. 2003;57:904–908. doi: 10.1038/sj.ejcn.1601624.
    1. Jarząb A., Kukula-Koch W. Recent advances in obesity: The role of turmeric tuber and its metabolites in the prophylaxis and therapeutical strategies. Curr. Med. Chem. 2017;24:1. doi: 10.2174/0929867324666161118095443.
    1. Chang Y.J., Myung S.-K., Chung S.T., Lee Y.K., Jeon Y.-J., Park C.-H., Seo H.G., Huh B.Y. Effects of vitamin treatment or supplements with purported antioxidant properties on skin cancer prevention: A meta-analysis of randomized controlled trials. Dermatology. 2011;223:36–44. doi: 10.1159/000329439.
    1. Puertollano M.A., Puertollano E., de Cienfuegos G.Á., de Pablo M.A. Dietary antioxidants: Immunity and host defense. Curr. Top. Med. Chem. 2011;11:1752–1766. doi: 10.2174/156802611796235107.
    1. Katta R., Brown D.C. Diet and skin cancer: The potential role of dietary antioxidants in nonmelanoma skin cancer prevention. J. Skin Cancer. 2015:893149. doi: 10.1155/2015/893149.
    1. Lugasi A., Hóvári J., Sági K.V., Bíró L. The role of antioxidant phytonutrients in the prevention of diseases. Acta Biol. Szeged. 2003;47:119–125.
    1. Grosso G., Micek A., Godos J., Pajak A., Sciacca S., Galvano F., Giovannucci E.L. Dietary flavonoid and lignan intake and mortality in prospective cohort studies: Systematic review and dose-response meta-analysis. Am. J. Epidemiol. 2017:1–13. doi: 10.1093/aje/kww207.
    1. Robbins R.J. Phenolic acids in foods: An overview of analytical methodology. J. Agric. Food Chem. 2003;51:2866–2887. doi: 10.1021/jf026182t.
    1. Koes R., Verweij W., Quattrocchio F. Flavonoids: A colourful model for the regulation and evolution of biochemical pathways. Trends Plant Sci. 2005;10:236–242. doi: 10.1016/j.tplants.2005.03.002.
    1. Hertog M.G.L., Hollman P.C.H., Venema D.P. Optimization of a quantitative HPLC determination of potentially anticarcinogenic flavonoids in vegetables and fruits. J. Agric. Food Chem. 1992;40:1591–1598. doi: 10.1021/jf00021a023.
    1. Yao L.H., Jiang Y.M., Shi J., Tomás-Barberán F.A., Datta N., Singanusong R., Chen S.S. Flavonoids in food and their health benefits. Plant Foods Hum. Nutr. 2004;59:113–122. doi: 10.1007/s11130-004-0049-7.
    1. Kühnau J. The flavonoids, a class of semi-essential food components: Their role in human nutrition. World Rev. Nutr. Diet. 1976;24:117–191. doi: 10.1159/000399407.
    1. Tomás-Barberán F.A., Clifford M.N. Flavanones, chalcones and dihydrochalcones-nature, occurrence and dietary burden. J. Sci. Food Agric. 2000;80:1073–1080. doi: 10.1002/(SICI)1097-0010(20000515)80:7<1073::AID-JSFA568>;2-B.
    1. Justesen U., Knuthsen P., Leth T. Determination of plant polyphenols in Danish foodstuffs by HPLC-UV and LC-MS detection. Cancer Lett. 1997;114:165–167. doi: 10.1016/S0304-3835(97)04651-X.
    1. Knekt P., Jarvinen R., Revnanen A., Moatela J. Flavonoid intake and coronary mortality in Finland: A cohort study. BMJ. 1996;312:478–481. doi: 10.1136/bmj.312.7029.478.
    1. Hertog M.G.L., Kromhout D., Aravanis C., Blackburn H., Buzina R., Fidanza F., Giampaoli S., Jansen A., Menotti A., Nedeljkovic S. Flavonoid intake and long term risk of coronary heart disease and cancer in the Seven Countries Study. Arch. Intern. Med. 1995;155:381–386. doi: 10.1001/archinte.1995.00430040053006.
    1. Rimm E.B., Katan M.B., Ascherio A., Stampfer M.J., Willett W.C. Relation between intake of flavonoids and risk for coronary heart disease in male health professionals. Ann. Intern. Med. 1996;12:384–389. doi: 10.7326/0003-4819-125-5-199609010-00005.
    1. Pozzo V., Goitre I., Fadda M., Gambion R., De Francesco A., Soldati L., Gentile L., Magistroni P., Cassader M., Bo S. Dietary flavonoid intake and cardiovascular risk: A population-based cohort study. J. Transl. Med. 2015;13:218. doi: 10.1186/s12967-015-0573-2.
    1. Pérez-Jiménez J., Neveu V., Vos F., Scalbert A. A systematic analysis of the content of 502 polyphenols in 452 foods and beverages—An application of the Phenol-Explorer database. J. Agric. Food Chem. 2010;58:4959–4969. doi: 10.1021/jf100128b.
    1. Neveu V., Pérez-Jiménez J., Vos F., Crespy V., Du Chaffaut L., Mennen L., Knox C., Eisner R., Cruz J., Wishart D., et al. Phenol-Explorer: An online comprehensive database on polyphenol contents in foods. Database. 2010;2010:bap024. doi: 10.1093/database/bap024.
    1. Pérez-Jiménez J., Neveu V., Vos F., Scalbert A. Identification of the 100 richest dietary sources of polyphenols: An application of the Phenol-Explorer database. Eur. J. Clin. Nutr. 2010;64:112–120. doi: 10.1038/ejcn.2010.221.
    1. Mishra A., Kumar S., Pandey A.K. Scientific validation of the medicinal efficacy of Tinospora cordifolia. Sci. World. J. 2013:292934. doi: 10.1155/2013/292934.
    1. Kukula-Koch W., Aligiannis N., Halabalaki M., Skaltsounis A.L., Glowniak K., Kalpoutzakis E. Influence of extraction procedures on phenolic content and antioxidant activity of Cretan barberry herb. Food Chem. 2013;138:406–413. doi: 10.1016/j.foodchem.2012.10.045.
    1. Kumar S., Mishra A. Chemistry and biological activities of flavonoids: An overview. Sci. World. J. 2013:162750. doi: 10.1155/2013/162750.
    1. Pinto M.S. Tea: A new perspective on health benefits. Food Res. Int. 2013;53:558–567. doi: 10.1016/j.foodres.2013.01.038.
    1. Bruno R.S., Bomser J.A., Ferruzzi M.G. Antioxidant Capacity of Green Tea (Camellia sinensis) In: Preedy V.R., editor. Processing and Impact on Antioxidants in Beverages. Academic Press; Oxford, UK: 2014.
    1. Kukula-Koch W., Koch W., Angelis A., Halabalaki M., Aligiannis N. Application of pH-zone refining hydrostatic countercurrent chromatography (hCCC) for the recovery of antioxidant phenolics and the isolation of alkaloids from Siberian barberry herb. Food Chem. 2016;203:394–401. doi: 10.1016/j.foodchem.2016.02.096.
    1. Sung H., Nah J., Chun S., Park H., Yang S.E., Min W.K. In vivo antioxidant effect of green tea. Eur. J. Clin. Nutr. 2000;54:527–529. doi: 10.1038/sj.ejcn.1600994.
    1. Arent S.M., Senso M., Golem D.L. The effects of theaflavin-enriched black tea extract on muscle soreness, oxidative stress, inflammation, and endocrine responses to acute anaerobic interval training: A randomized, double-blind, crossover study. J. Int. Soc. Sport. Nutr. 2010;7:11. doi: 10.1186/1550-2783-7-11.
    1. Imran A., Arshad M.U., Arshad M.S., Imran M., Saeed F., Sohaib M. Lipid peroxidation diminishing perspective of isolated theaflavins and thearubigins from black tea in arginine induced renal malfunctional rats. Lipid. Health. Dis. 2018;17:157. doi: 10.1186/s12944-018-0808-3.
    1. Tsai P.H., Kan N.B., Ho S.C., Liu C.C., Lin C.C. Effects of oolong tea supplementationon lipid peroxidation of athletes at rest and post-exhaustive exercise. J. Food Sci. 2005;70:581–585. doi: 10.1111/j.1365-2621.2005.tb08332.x.
    1. Weerawatanakorn M., Hung W.-L., Pan M.-H., Li S., Li D., Wan X., Ho C.-T. Chemistry and health beneficial effects of oolong tea and theasinensins. Food Sci. Hum. Well. 2015;4:133–146. doi: 10.1016/j.fshw.2015.10.002.
    1. Pae M., Wu D. Immunomodulating effect of epigallocatechin-3-gallate from green tea: Mechanisms and applications. Food Funct. 2013;4:1287–1303. doi: 10.1039/c3fo60076a.
    1. Wu D. Green tea EGCG, T-cell function, and T-cell-mediated autoimmune encephalomyelitis. J. Investig. Med. 2016;64:1213–1219. doi: 10.1136/jim-2016-000158.
    1. Lee S.Y., Jung Y.O., Ryu J.G., Oh H.J., Son H.J., Lee S.H., Kwon J.E., Kim E.K., Park M.K., Park S.H., et al. Epigallocatechin-3-gallate ameliorates autoimmune arthritis by reciprocal regulation of T helper-17 regulatory T cells and inhibition of osteoclastogenesis by inhibiting STAT3 signaling. J. Leucoc. Biol. 2016;100:559–568. doi: 10.1189/jlb.3A0514-261RR.
    1. Nikfarjam B.A., Adineh M., Hajiali F., Nassiri-Asl M. Treatment with rutin—A therapeutic strategy for neutrophil-mediated inflammatory and autoimmune diseases: Anti-inflammatory effects of rutin on neutrophils. J. Pharmacopunct. 2017;20:52–56. doi: 10.3831/KPI.2017.20.003.
    1. Nikfarjam B.A., Hajiali F., Adineh M., Nassiri-Asl M. Anti-inflammatory Effects of Quercetin and Vitexin on Activated Human Peripheral Blood Neutrophils. J. Pharmacopunct. 2017;20:127–131. doi: 10.3831/KPI.2017.20.017.
    1. Zhang S., Liu X., Sun C., Yang J., Wang L., Liu J., Gong L., Jing Y. Apigenin attenuates experimental autoimmune myocarditis by modulating Th1/Th2 cytokine balance in mice. Inflammation. 2016;39:678–686. doi: 10.1007/s10753-015-0294-y.
    1. Zhang Y., Duan W., Owusu L., Wu D., Xin Y. Epigallocatechin-3-gallate induces the apoptosis of hepatocellular carcinoma LM6 cells but not non-cancerous liver cells. Int. J. Mol. Med. 2015;35:117–124. doi: 10.3892/ijmm.2014.1988.
    1. Sur S., Pal D., Roy R., Barua A., Roy A., Saha P., Panda C.K. Tea polyphenols EGCG and TF restrict tongue and liver carcinogenesis simultaneously induced by N-nitrosodiethylamine in mice. Toxicol. Appl. Pharmacol. 2016;300:34–46. doi: 10.1016/j.taap.2016.03.016.
    1. Kalra N., Seth K., Prasad S., Singh M., Pant A.B., Shukla Y. Theaflavins induced apoptosis of LNCaP cells is mediated through induction of p53, down-regulation of NF-kappa B and mitogen-activated protein kinases pathways. Life Sci. 2007;80:2137–2146. doi: 10.1016/j.lfs.2007.04.009.
    1. Prasad S., Kaur J., Roy P., Kalra N., Shukla Y. Theaflavins induce G2/M arrest by modulating expression of p21waf1/cip1, cdc25C and cyclin B in human prostate carcinoma PC-3 cells. Life Sci. 2007;81:1323–1331. doi: 10.1016/j.lfs.2007.07.033.
    1. He H.-F. Research progress on theaflavins: Efficacy, formation, and preparation. Food Nutr. Res. 2017;61:1344521. doi: 10.1080/16546628.2017.1344521.
    1. Song W., Zhao X., Xu J., Zhang H. Quercetin inhibits angiogenesis-mediated human retinoblastoma growth by targeting vascular endothelial growth factor receptor. Oncol. Lett. 2017;14:3343–3348. doi: 10.3892/ol.2017.6623.
    1. Hashemzaei M., Far A.D., Yari A., Heravi R.E., Tabrizian K., Taghdisi S.M., Sadegh S.E., Tsarouhas K., Kouretas D., Tzanakakis G., et al. Anticancer and apoptosis-inducing effects of quercetin in vitro and in vivo. Oncol. Rep. 2017;38:819–828. doi: 10.3892/or.2017.5766.
    1. Dai J., Van Wie P.G., Fai L.Y., Kim D., Wang L., Poyil P., Luo J., Zhang Z. Downregulation of NEDD9 by apigenin suppresses migration, invasion, and metastasis of colorectal cancer cells. Toxicol. Appl. Pharmacol. 2016;311:106–112. doi: 10.1016/j.taap.2016.09.016.
    1. Tseng T.H., Chien M.H., Lin W.L., Wen Y.C., Chow J.M., Chen C.K., Kuo T.C., Lee W.J. Inhibition of MDA-MB-231 breast cancer cell proliferation and tumor growth by apigenin through induction of G2/M arrest and histone H3 acetylation-mediated p21WAF1/CIP1 expression. Environ. Toxicol. 2017;32:434–444. doi: 10.1002/tox.22247.
    1. Shukla S., Fu P., Gupta S. Apigenin induces apoptosis by targeting inhibitor of apoptosis proteins and Ku70-Bax interaction in prostate cancer. Apoptosis. 2014;19:883–894. doi: 10.1007/s10495-014-0971-6.
    1. Shukla S., Shankar E., Fu P., MacLennan G.T., Gupta S. Suppression of NF-κB and NF-κB-Regulated gene expression by apigenin through IκBα and IKK pathway in TRAMP mice. PLoS ONE. 2015;10:e0138710. doi: 10.1371/journal.pone.0138710.
    1. Cao H.H., Chu J.H., Kwan H.Y., Su T., Yu H., Cheng C.Y., Fu X.Q., Guo H., Li T., Tse A.K., et al. Inhibition of the STAT3 signaling pathway contributes to apigenin-mediated anti-metastatic effect in melanoma. Sci. Rep. 2016;6:21731. doi: 10.1038/srep21731.
    1. Hu X.W., Meng D., Fang J. Apigenin inhibited migration and invasion of human ovarian cancer A2780 cells through focal adhesion kinase. Carcinogenesis. 2008;29:2369–2376. doi: 10.1093/carcin/bgn244.
    1. Meng S., Zhu Y., Li J.F., Wang X., Liang Z., Li S.Q., Xu X., Chen H., Liu B., Zheng X.Y., et al. Apigenin inhibits renal cell carcinoma cell proliferation. Oncotarget. 2017;8:19834–19842. doi: 10.18632/oncotarget.15771.
    1. Banjerdpongchai R., Wudtiwai B., Khaw-on P., Rachakhom W., Duangnil N., Kongtawelert P. Hesperidin from Citrus seed induces human hepatocellular carcinoma HepG2 cell apoptosis via both mitochondrial and death receptor pathways. Tumour Biol. 2016;37:227–237. doi: 10.1007/s13277-015-3774-7.
    1. Lee C.J., Wilson L., Jordan M.A., Nguyen V., Tang J., Smiyun G. Hesperidin suppressed proliferations of both human breast cancer and androgen-dependent prostate cancer cells. Phytother. Res. 2010;24:15–19. doi: 10.1002/ptr.2856.
    1. Zhao J., Li Y., Gao J., De Y. Hesperidin inhibits ovarian cancer cell viability through endoplasmic reticulum stress signaling pathways. Oncol. Lett. 2017;14:5569–5574. doi: 10.3892/ol.2017.6873.
    1. González-Sarrías A., Combet E., Pinto P., Mena P., Dall’Asta M., Garcia-Aloy M., Rodríguez-Mateos A., Gibney E.R., Dumont J., Massaro M., et al. A systematic review and meta-analysis of the effects of flavanol-containing tea, cocoa and apple products on body composition and blood lipids: Exploring the factors responsible for variability in their efficacy. Nutrients. 2017;9:746. doi: 10.3390/nu9070746.
    1. Bogdanski P., Suliburska J., Szulinska M., Stepien M., Pupek-Musialik D., Jablecka A. Green tea extract reduces blood pressure, inflammary biomarkers, and oxidative stress and improves, parameters associated with insulin resistance in obese, hypertensive patients. Nutr. Res. 2012;32:421–427. doi: 10.1016/j.nutres.2012.05.007.
    1. Ademiluyi A.O., Oboh G., Ogunsuyi O.B., Oloruntoba F.M. A comparative study on antihypertensive and antioxidant properties of phenolic extracts from fruit and leaf of some guava (Psidium guajava L.) varieties. Comp. Clin. Pathol. 2016;25:363–374. doi: 10.1007/s00580-015-2192-y.
    1. Tounekti T., Joubert E., Hernandez I., Munne-Bosch S. Improving the polyphenol content of tea. Crit. Rev. Plant Sci. 2013;32:192–215. doi: 10.1080/07352689.2012.747384.
    1. Gómez-Guzmán M., Jiménez R., Sánchez M., Zarzuelo M.J., Galindo P., Quintela A.M., Lopez-Sepulveda R., Romero M., Tamargo J., Vargas F., et al. Epicatechin lowers blood pressure, restores endothelial function, and decreases oxidative stress and endothelin-1 and NADPH oxidase activity in DOCA-salt hypertension. Free Radic. Biol. Med. 2012;52:70–79. doi: 10.1016/j.freeradbiomed.2011.09.015.
    1. Mahajan N., Dhawan V., Sharma G., Jain S., Kaul D. Induction of inflammatory gene expression by THP-1 macrophages cultured in normocholesterolaemic hypertensive sera and modulatory effects of green tea polyphenols. J. Hum. Hypertens. 2008;22:141–143. doi: 10.1038/sj.jhh.1002277.
    1. Chen X.Q., Hu T., Han Y., Huang W., Yuan H.B., Zhang Y.T., Du Y., Jiang Y.W. Preventive Effects of Catechins on Cardiovascular Disease. Molecules. 2016;21:1759. doi: 10.3390/molecules21121759.
    1. Namkung W., Thiagarajah J.R., Phuan P.W., Verkman A.S. Inhibition of Ca2+-activated Cl¯ channels by gallotannins as a possible molecular basis for health benefits of red wine and green tea. FASEB J. 2010;24:4178–4186. doi: 10.1096/fj.10-160648.
    1. Ohno S., Yokoi H., Mori K., Kasahara M., Kuwahara K., Fujikura J., Naito M., Kuwabara T., Imamaki H., Ishii A., et al. Ablation of the N-type calcium channel ameliorates diabetic nephropathy with improved glycemic control and reduced blood pressure. Sci. Rep. 2016;6:27192. doi: 10.1038/srep27192.
    1. Potenza M.A., Marasciulo F.L., Tarquinio M., Tiravanti E., Colantuono G., Federici A., Kim J.A., Quon M.J., Montagnani M. EGCG, a green tea polyphenol, improves endothelial function and insulin sensitivity, reduces blood pressure, and protects against myocardial I/R injury in SHR. Am. J. Physiol. Endocrinol. Metab. 2007;292:1378–1387. doi: 10.1152/ajpendo.00698.2006.
    1. Li F., Takahashi Y., Yamaki K. Inhibitory effect of catechin-related compounds on renin activity. Biomed. Res. 2013;34:167–171. doi: 10.2220/biomedres.34.167.
    1. Huang J., Wang Y., Xie Z., Zhou Y., Zhang Y., Wan X. The anti-obesity effects of green tea in human intervention and basic molecular studies. Eur. J. Clin. Nutr. 2014;68:1075–1087. doi: 10.1038/ejcn.2014.143.
    1. Moon H.S., Lee H.G., Choi Y.J., Kim T.G., Cho C.S. Proposed mechanisms of (-)-epigallocatechin-3-gallate for anti-obesity. Chem. Biol. Interact. 2007;167:85–98. doi: 10.1016/j.cbi.2007.02.008.
    1. Bose M., Lambert J.D., Ju J., Reuhl K.R., Shapses S.A., Yang C.S. The major green tea polyphenol, (-)-epigallocatechin-3 gallate, inhibits obesity, metabolic syndrome, and fatty liver disease in high-fat-fed mice. J. Nutr. 2008;138:1677–1683. doi: 10.1093/jn/138.9.1677.
    1. Nagao T., Hase T., Tokimitsu I. A green tea extract high in catechins reduces body fat and cardiovascular risks in humans. Obesity. 2007;15:1473–1483. doi: 10.1038/oby.2007.176.
    1. Mehta V., Parashar A., Sharma A., Singh T.R., Udayabanu M. Quercetin ameliorates chronic unpredicted stress-mediated memory dysfunction in male Swiss albino mice by attenuating insulin resistance and elevating hippocampal GLUT4 levels independent of insulin receptor expression. Horm Behav. 2017;89:13–22. doi: 10.1016/j.yhbeh.2016.12.012.
    1. Cialdella-Kam L., Ghosh S., Meaney M.P., Knab A.M., Shanely R.A., Nieman D.C. Quercetin and green tea extract supplementation downregulated genes related to tissue inflammatory responses to a 12-week high fat-diet in mice. Nutrients. 2017;9:773. doi: 10.3390/nu9070773.
    1. Henagan T.M., Lenard N.R., Gettys T.W., Stewart L.K. Dietary quercetin supplementation in mice increases skeletal muscle PGC1alpha expression, improves mitochondrial function and attenuates insulin resistance in a time-specific manner. PLoS ONE. 2014;9:e89365. doi: 10.1371/journal.pone.0089365.
    1. Jung C.H., Cho I., Ahn J., Jeon T.-I., Ha T.-Y. Quercetin reduces high-fat diet-induced fat accumulation in the liver by regulating lipid metabolism genes. Phytother. Res. 2013;27:139–143. doi: 10.1002/ptr.4687.
    1. Ding L., Jin D., Chen X. Luteolin enhances insulin sensitivity via activation of PPARγ transcriptional activity in adipocytes. J. Nutr. Biochem. 2010;21:941–947. doi: 10.1016/j.jnutbio.2009.07.009.
    1. Jaacks L.M., Siegel K.R., Gujral U.P., Narayan K.M. Type 2 diabetes: A 21st century epidemic. Best Pract. Res. Clin. Endocrinol. Metab. 2016;30:331–343. doi: 10.1016/j.beem.2016.05.003.
    1. Rauter A.P., Martins A., Borges C., Mota-Filipe H., Pinto R., Sepodes B., Justino J. Antihyperglycaemic and protective effects of flavonoids on streptozotocin-induced diabetic rats. Phytother. Res. 2010;24:133–138. doi: 10.1002/ptr.3017.
    1. Zang M., Xu S., Maitland-Toolan K.A., Zuccollo A., Hou X., Jiang B., Wierzbicki M., Verbeuren T.J., Cohen R.A. Polyphenols stimulate amp-activated protein kinase, lower lipids, and inhibit accelerated atherosclerosis in diabetic ldl receptor-deficient mice. Diabetes. 2006;55:2180–2191. doi: 10.2337/db05-1188.
    1. Hossain M.K., Dayem A.A., Han J., Yin Y., Kim K., Saha S.K., Yang G.-M., Choi H.Y., Cho S.-G. Molecular mechanism of the anti-obesity and anti-diabetic properties of flavonoids. Int. J. Mol. Sci. 2016;17:569. doi: 10.3390/ijms17040569.
    1. Panda S., Kar A. Apigenin (4′,5,7-trihydroxyflavone) regulates hyperglycaemia, thyroid dysfunction and lipid peroxidation in alloxan induced diabetic mice. J. Pharm. Pharmacol. 2007;59:1543–1548. doi: 10.1211/jpp.59.11.0012.
    1. Suh K.S., Oh S., Woo J.-T., Kim S.-W., Kim J.-W., Kim Y.S., Chon S. Apigenin attenuates 2-deoxy-d-ribose-induced oxidative cell damage in HIT-T15 pancreatic. β-cells. Biol. Pharm. Bull. 2012;35:121–126. doi: 10.1248/bpb.35.121.
    1. Jung U.J., Lee M.K., Park Y.B., Kang M.A., Choi M.S. Effect of citrus flavonoids on lipid metabolism and glucose-regulating enzyme mRNA levels in type-2 diabetic mice. Int. J. Biochem. Cell Biol. 2006;38:1134–1145. doi: 10.1016/j.biocel.2005.12.002.
    1. Pu P., Gao D.-M., Mohamed S., Chen J., Zhang J., Zhou X.-Y., Zhou N.-J., Xie J., Jiang H. Naringin ameliorates metabolic syndrome by activating amp-activated protein kinase in mice fed a high-fat diet. Arch. Biochem. Biophys. 2012;518:61–70. doi: 10.1016/j.abb.2011.11.026.
    1. Koch C.E., Ganjam G.K., Steger J., Legler K., Stohr S., Schumacher D., Hoggard N., Heldmaier G., Tups A. The dietary flavonoids naringenin and quercetin acutely impair glucose metabolism in rodents possibly via inhibition of hypothalamic insulin signalling. Br. J. Nutr. 2013;109:1040–1051. doi: 10.1017/S0007114512003005.
    1. Akiyama S., Katsumata S., Suzuki K., Ishimi Y., Wu J., Uehara M. Dietary hesperidin exerts hypoglycemic and hypolipidemic effects in streptozotocin-induced marginal type 1 diabetic rats. J. Clin. Biochem. Nutr. 2010;46:87–92. doi: 10.3164/jcbn.09-82.
    1. Jung U.J., Lee M.-K., Jeong K.-S., Choi M.-S. The hypoglycemic effects of hesperidin and naringin are partly mediated by hepatic glucose-regulating enzymes in C57BL/KsJ-db/db mice. J. Nutr. 2004;134:2499–2503. doi: 10.1093/jn/134.10.2499.
    1. Jung U.J., Choi M.-S. Obesity and its metabolic complications: The role of adipokines and the relationship between obesity, inflammation, insulin resistance, dyslipidemia and nonalcoholic fatty liver disease. Int. J. Mol. Sci. 2014;15:6184–6223. doi: 10.3390/ijms15046184.
    1. Agrawal Y.O., Sharma P.K., Shrivastava B., Ojha S., Upadhya H.M., Arya D.S., Goyal S.N. Hesperidin produces cardioprotective activity via PPAR- pathway in ischemic heart disease model in diabetic rats. PLoS ONE. 2014;9:e111212. doi: 10.1371/journal.pone.0111212.
    1. Eid H.M., Martineau L.C., Saleem A., Muhammad A., Vallerand D., Benhaddou-Andaloussi A., Nistor L., Afshar A., Arnason J.T., Haddad P.S. Stimulation of AMP-activated protein kinase and enhancement of basal glucose uptake in muscle cells by quercetin and quercetin glycosides, active principles of the antidiabetic medicinal plant vaccinium vitis-idaea. Mol. Nutr. Food Res. 2010;54:991–1003. doi: 10.1002/mnfr.200900218.
    1. Alam M.M., Meerza D., Naseem I. Protective effect of quercetin on hyperglycemia, oxidative stress and DNA damage in alloxan induced type 2 diabetic mice. Life Sci. 2014;109:8–14. doi: 10.1016/j.lfs.2014.06.005.
    1. Kobori M., Masumoto S., Akimoto Y., Takahashi Y. Dietary quercetin alleviates diabetic symptoms and reduces streptozotocin-induced disturbance of hepatic gene expression in mice. Mol. Nutr. Food Res. 2009;53:859–868. doi: 10.1002/mnfr.200800310.
    1. Xu M., Hu J., Zhao W., Gao X., Jiang C., Liu K., Liu B., Huang F. Quercetin differently regulates insulin-mediated glucose transporter 4 translocation under basal and inflammatory conditions in adipocytes. Mol. Nutr. Food Res. 2014;58:931–941. doi: 10.1002/mnfr.201300510.
    1. Prince P., Kamalakkannan N. Rutin improves glucose homeostasis in streptozotocin diabetic tissues by altering glycolytic and gluconeogenic enzymes. J. Biochem. Mol. Toxicol. 2006;20:96–102. doi: 10.1002/jbt.20117.
    1. Jeong S.M., Kang M.J., Choi H.N., Kim J.H., Kim J.I. Quercetin ameliorates hyperglycemia and dyslipidemia and improves antioxidant status in type 2 diabetic db/db mice. Nutr. Res. Pract. 2012;6:201–207. doi: 10.4162/nrp.2012.6.3.201.
    1. Arias N., Macarulla M.T., Aguirre L., Martinez-Castano M.G., Portillo M.P. Quercetin can reduce insulin resistance without decreasing adipose tissue and skeletal muscle fat accumulation. Genes Nutr. 2014;9:361. doi: 10.1007/s12263-013-0361-7.
    1. Yang X., Kong F. Evaluation of the in vitro α-glucosidase inhibitory activity of green tea polyphenols and different tea types. J. Sci. Food Agric. 2016;96:777–782. doi: 10.1002/jsfa.7147.
    1. Johnston K., Sharp P., Clifford M., Morgan L. Dietary polyphenols decrease glucose uptake by human intestinal Caco-2 cells. FEBS Lett. 2005;579:1653–1657. doi: 10.1016/j.febslet.2004.12.099.
    1. Mandel S., Grunblatt E., Riederer P., Gerlach M., Levites Y., Youdim M.B.H. Neuroprotective strategies in Parkinson’s disease: An update on progress. CNS Drugs. 2003;17:729–762. doi: 10.2165/00023210-200317100-00004.
    1. Berg D., Gerlach M., Youdim M.B.H., Double K.L., Zecca L., Riederer P., Becker G. Brain iron pathways and their relevance to Parkinson’s disease. J. Neurochem. 2001;79:225–236. doi: 10.1046/j.1471-4159.2001.00608.x.
    1. Dauer W., Przedborski S. Parkinson’s disease: Mechanisms and models. Neuron. 2003;39:889–909. doi: 10.1016/S0896-6273(03)00568-3.
    1. Cardoso S.M., Moreira P.I., Agostinho P., Pereira C., Oliveira C.R. Neurodegenerative pathways in Parkinson’s disease: Therapeutic strategies. Curr. Drug Targets CNS Neurol. Disord. 2005;4:405–419. doi: 10.2174/1568007054546072.
    1. Braak H., Ghebremedhin E., Rüb U., Bratzke H., Del Tredici K. Stages in the development of Parkinson’s disease-related pathology. Cell Tissue Res. 2004;318:121–134. doi: 10.1007/s00441-004-0956-9.
    1. McGeer P.L., Itagaki S., Akiyama H., McGeer E.G. Rate of cell death in parkinsonism indicates active neuropathological process. Ann. Neurol. 1988;24:574–576. doi: 10.1002/ana.410240415.
    1. Miller R.L., James-Kracke M., Sun G.Y., Sun A.Y. Oxidative and inflammatory pathways in Parkinson’s disease. Neurochem. Res. 2009;34:55–65. doi: 10.1007/s11064-008-9656-2.
    1. Hamaguchi T., Ono K., Murase A., Yamada M. Phenolic compounds prevent Alzheimer’s pathology through different effects on the amyloid-beta aggregation pathway. Am. J. Pathol. 2009;175:2557–2565. doi: 10.2353/ajpath.2009.090417.
    1. Smith A., Giunta B., Bickford P.C., Fountain M., Tan J., Shytle R.D. Nanolipidic particles improve the bioavailability and alpha-secretase inducing ability of epigallocatechin-3-gallate (EGCG) for the treatment of Alzheimer’s disease. Int. J. Pharm. 2010;389:207–212. doi: 10.1016/j.ijpharm.2010.01.012.
    1. Janle M.E., Lila M.A., Grannan M., Wood L., Higgins A., Yousef G.G., Rogers R.B., Kim H., Jackson G.S., Ho L., et al. Pharmacokinetics and tissue distribution of 14C-labeled grape polyphenols in the periphery and the central nervous system following oral administration. J. Med. Food. 2010;13:926–933. doi: 10.1089/jmf.2009.0157.
    1. Stevenson D.E., Hurst R.D. Polyphenolic phytochemicals—Just antioxidants or much more? Cell Mol. Life Sci. 2007;64:2900–2916. doi: 10.1007/s00018-007-7237-1.
    1. Fraga C.G. Plant polyphenols: How to translate their in vitro antioxidant actions to in vivo conditions. Life. 2007;59:308–315. doi: 10.1080/15216540701230529.
    1. Karpinar D.P., Balija M.B., Kügler S., Opazo F., Rezaei-Ghaleh N., Wender N., Kim H.Y., Taschenberger G., Falkenburger B.H., Heise H., et al. Pre-fibrillar alpha-synuclein variants with impaired beta-structure increase neurotoxicity in Parkinson’s disease models. EMBO J. 2009;28:3256–3268. doi: 10.1038/emboj.2009.257.
    1. Marques O., Outeiro T.F. Alpha-synuclein: From secretion to dysfunction and death. Cell Death Dis. 2012;3:e350. doi: 10.1038/cddis.2012.94.
    1. Masuda M., Suzuki N., Taniguchi S., Oikawa T., Nonaka T., Iwatsubo T., Hisanaga S., Goedert M., Hasegawa M. Small molecule inhibitors of alpha-synuclein filament assembly. Biochemistry. 2006;45:6085–6094. doi: 10.1021/bi0600749.
    1. Meng X., Munishkina L.A., Fink A.L., Uversky V.N. Effects of various flavonoids on the alpha-synuclein fibrillation process. Parkinsons Dis. 2010;650794:1–16. doi: 10.4061/2010/650794.
    1. Ehrnhoefer D.E., Bieschke J., Boeddrich A., Herbst M., Masino L., Lurz R., Engemann S., Pastore A., Wanker E.E. EGCG redirects amyloidogenic polypeptides into unstructured, off-pathway oligomers. Nat. Struct. Mol. Biol. 2008;15:558–566. doi: 10.1038/nsmb.1437.
    1. Bae S.Y., Kim S., Hwang H., Kim H.K., Yoon H.C., Kim J.H., Lee S., Kim T.D. Amyloid formation and disaggregation of alpha-synuclein and its tandem repeat (alpha-TR) Biochem. Biophys. Res. Commun. 2010;400:531–536. doi: 10.1016/j.bbrc.2010.08.088.
    1. Bieschke J., Russ J., Friedrich R.P., Ehrnhoefer D.E., Wobst H., Neugebauer K., Wanker E.E. EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicity. Proc. Natl. Acad. Sci. USA. 2010;107:7710–7715. doi: 10.1073/pnas.0910723107.
    1. Lu H., Meng X., Yang C.S. Enzymology of methylation of tea catechins and inhibition of catechol-O-methyltransferase by (−)-epigallocatechin gallate. Drug Metab. Dispos. 2003;31:572–579. doi: 10.1124/dmd.31.5.572.
    1. Levites Y., Weinreb O., Maor G., Youdim M.B.H., Mandel S. Green tea polyphenol (-)-epigallocatechin-3-gallate prevents N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced dopaminergic neurodegeneration. J. Neurochem. 2001;78:1073–1082. doi: 10.1046/j.1471-4159.2001.00490.x.
    1. Mandel S., Maor G., Youdim M.B.H. Iron and alpha synuclein in the substantia nigra of MPTP-treated mice: Effect of neuroprotective drugs R-apomorphine and green tea polyphenol epigallocatechin-3-gallate. J. Mol. Neurosci. 2004;24:401–416. doi: 10.1385/JMN:24:3:401.
    1. Chaturvedi R.K., Shukla S., Seth K., Chauhan S., Sinha C., Shukla Y., Agrawal A.K. Neuroprotective and neurorescue effect of black tea extract in 6-hydroxydopamine-lesioned rat model of Parkinson’s disease. Neurobiol. Dis. 2006;22:421–434. doi: 10.1016/j.nbd.2005.12.008.
    1. Checkoway H., Powers K., Smith-Weller T., Franklin G.M., Longstreth W.T., Jr., Swanson P.D. Parkinson’s disease risks associated with cigarette smoking, alcohol consumption, and caffeine intake. Am. J. Epidemiol. 2002;155:732–738. doi: 10.1093/aje/155.8.732.
    1. Gao X., Cassidy A., Schwarzschild M.A., Rimm E.B., Ascherio A. Habitual intake of dietary flavonoids and risk of Parkinson disease. Neurology. 2012;78:1138–1145. doi: 10.1212/WNL.0b013e31824f7fc4.
    1. Baptista F.I., Henriques A.G., Silva A.M.S., Wiltfang J., da Cruz a Silva O.A.B. Flavonoids as therapeutic compounds targeting key proteins involved in Alzehimer’s disease. ACS Chem. Neurosci. 2014;5:83–92. doi: 10.1021/cn400213r.
    1. Van Cauwenberghe C., Van Broeckhoven C., Sleegers K. The genetic landscape of Alzheimer disease: Clinical implications and perspectives. Genet. Med. 2015;18:421–430. doi: 10.1038/gim.2015.117.
    1. Mendiola-Precoma J., Berumen L.C., Padilla K., Garcia-Alcocer G. Therapies for prevention and treatment of Alzheimer’s disease. Biomed. Res. Int. 2016:2589276. doi: 10.1155/2016/2589276.
    1. Contestabile A. The history of the cholinergic hypothesis. Behav. Brain Res. 2011;221:334–340. doi: 10.1016/j.bbr.2009.12.044.
    1. Cervellati C., Wood P.L., Romani A., Valacchi G., Squerzanti M., Sanz J.M., Ortolani B., Zuliani G. Oxidative challenge in Alzheimer’s disease: State of knowledge and future needs. J. Investig. Med. 2016;64:21–32. doi: 10.1136/jim-2015-000017.
    1. Folch J., Patraca I., Martínez N., Pedrós I., Petrov D., Ettcheto M., Abad S., Marin M., Beas-Zarate C., Camins A. The role of leptin in the sporadic form of Alzheimer’s disease. Interactions with the adipokines amylin, ghrelin and the pituitary hormone prolactin. Life Sci. 2015;140:19–28. doi: 10.1016/j.lfs.2015.05.002.
    1. Talbot K., Wang H.Y., Kazi H., Han L.Y., Bakshi K.P., Stucky A., Fuino R.L., Kawaguchi K.R., Samoyedny A.J., Wilson R.S., et al. Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. J. Clin. Investig. 2012;122:1316–1338. doi: 10.1172/JCI59903.
    1. Commenges D., Scotet V., Renaud S., Jacqmin-Gadda H., Barberger-Gateau P., Dartigues J.F. Intake of flavonoids and risk of dementia. J. Epidemiol. 2000;16:357–363. doi: 10.1023/A:1007614613771.
    1. Le Bars P.L., Kieser M., Itil K.Z. A 26-week analysis of a double-blind, placebo-controlled trial of the ginkgo biloba extract EGb 761 in dementia. Dement. Geriatr. Cognit. Disord. 2000;11:230–237. doi: 10.1159/000017242.
    1. Youdim K.A., Joseph J.A. A possible emerging role of phytochemicals in improving age-related neurological dysfunctions: A multiplicity of effects. Free Radic. Biol. Med. 2001;30:583–594. doi: 10.1016/S0891-5849(00)00510-4.
    1. Joseph J.A., Denisova N.A., Arendash G., Gordon M., Diamond D., Shukitt-Hale B., Morgan D. Blueberry supplementation enhances signaling and prevents behavioral deficits in an Alzheimer disease model. Nat. Neurosci. 2003;6:153–162. doi: 10.1080/1028415031000111282.
    1. Levites Y., Amit T., Mandel S., Youdim M.B.H. Neuroprotection and neurorescue against amyloid beta toxicity and PKC-dependent release of non-amyloidogenic soluble precursor protein by green tea polyphenol (-)-epigallocatechin-3-gallate. FASEB J. 2003;17:952–954. doi: 10.1096/fj.02-0881fje.
    1. Ono K., Yoshiike Y., Takashima A., Hasegawa K., Naiki H., Yamada M. Potent anti-amyloidogenic and fibril-destabilizing effects of polyphenols in vitro: Implications for the prevention and therapeutics of Alzheimer’s disease. J. Neurochem. 2003;87:172–181. doi: 10.1046/j.1471-4159.2003.01976.x.
    1. Morris M.S. Homocysteine and Alzheimer’s disease. Lancet. Neurol. 2003;7:425–428. doi: 10.1016/S1474-4422(03)00438-1.
    1. Wojtunik-Kulesza K.A., Oniszczuk A., Oniszczuk T., Waksmundzka-Hajnos M. The influence of common free radicals and antioxidants on development of Alzheimer’s Disease. Biomed. Pharmacother. 2016;78:39–45. doi: 10.1016/j.biopha.2015.12.024.
    1. Dai Q., Borenstein A.R., Wu Y., Jackson J.C., Larson E.B. Fruit and vegetable juices and Alzheimer’s disease: The Kame Project. Am. J. Med. 2006;119:751–759. doi: 10.1016/j.amjmed.2006.03.045.
    1. Wang J., Zhao Z., Ho L., Seror I., Humala N., Percival S. Moderate consumption of Cabernet Sauvignon attenuates β-amyloid neuropathology in a mouse model of Alzheimer’s disease. FASEB J. 2006;20:2313–2320. doi: 10.1096/fj.06-6281com.
    1. Luchsinger J.A., Tang M.-X., Siddiqui M., Shea S., Mayeux R. Alcohol intake and risk of dementia. J. Am. Geriatr. Soc. 2004;52:540–546. doi: 10.1111/j.1532-5415.2004.52159.x.

Source: PubMed

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