Further randomized controlled trials are needed to confirm the promising protective effects of polyphenols on CVD and establish dietary recommendations and desired minimum levels of intake.

Tresserra-Rimbau, E. Rimm, A. Medina-Remon, et al. on behalf of the PREDIMED Study Investigators. Show more.

Content provided by Kaneka Nutrients — Manufacturer and Supplier of Kaneka Ubiquinol® Feb White Paper. An ally in the fight against oxidative stress, Kaneka Ubiquinol® offers antioxidant support for men and women concerned about reproductive health. Content provided by Enovate Biolife LLC Jan White Paper.

Content provided by DolCas Biotech, LLC. Viable natural product options for "healthy weight management" in the age of Ozempic and other GLP-1 inhibitors will require targeted innovations In addition, prehypertension is already prevalent and accompanied by increased aortic stiffness, impaired elasticity, decreased cardiac function, and diminished insulin resistance Hence, hypertension is not only a chronic form of CVD but also worsens the morbidity and mortality of major CVD Abnormal fasting plasma glucose FPG increases the risk of CVD Abnormal glucose metabolism, especially hyperglycemia, leads to oxidative stress, microvascular damage, vascular tone and endothelial damage, as well as platelet aggregation and embolism 37 , In addition, hyperglycemia induces certain inflammatory factors [tumor necrosis factor-α TNF-α , interleukin-6 IL-6 , C-reactive protein CRP , etc.

Lipids are the general term for neutral fats [triacylglycerols TG and total cholesterol TC ] and lipids in plasma phospholipids, glycolipids, sterols, and steroids , which are essential for the basic metabolism of living cells Among them, cholesterol [low density lipoprotein LDL and high density lipoprotein HDL ] and TG are closely related to the development of atherosclerosis AS 40 , Tobacco contains approximately 4, chemicals, of which nicotine, carbon monoxide and other components stimulate blood pressure, lead to coronary AS, increase blood and platelet viscosity, reduce the ability to dissolve blood clots and oxygen-carrying capacity of hemoglobin, and even induce ventricular fibrillation, increasing the incidence of cardiovascular events 46 , Many studies now indicate that small amounts of alcohol consumption can moderately reduce the risk of myocardial infarction 48 , However, the effects of heavy alcohol use on exacerbating CVD cannot be ignored.

Both long-term heavy drinking and occasional heavy drinking can, to varying degrees, decrease HDL-C, increase plasma viscosity and fibrinogen concentration, cause platelet aggregation, impair endothelial function, increase inflammatory responses, increase heart rate, and inhibit cardiac contractile function, thereby increasing the incidence of CVD, morbidity and mortality 50 , The structure, quantity, and type of diet can also influence the occurrence of cardiovascular events 52 , For example, a high-salt diet can exacerbate vasoconstriction, leading to elevated blood pressure and plasma cholesterol and contributing to the development of AS 52 — Sugar can increase blood viscosity and slow blood flow, which, combined with damage to the vascular endothelium, causes the generation of a large number of atherosclerotic plaques that block blood vessels and trigger the occurrence of acute cardiovascular events 56 , A high-fat diet can cause obesity or overweight, leading to metabolic disorders such as hyperlipidemia, hypertension, and other CVDs 58 , It is reported that in patients with insomnia, serum HDL is low, while TG level is high 60 , In addition, CVDs are closely related to psychological conditions such as depression, chronic psychological stress, post traumatic stress disorder PTSD , and anxiety Numerous epidemiological studies have shown that sex, age, and family history influence the incidence and mortality rates of CVD 63 , Moreover, the prevalence and mortality rates are higher in men than in women, especially in premenopausal women Postmenopausal women lack the protective mechanisms of a specific physiological period, and with the decrease in estrogen levels, the metabolism of the body changes, leading to an increase in the incidence of CVD 65 , As a natural polyphenol complex, TPs are characterized by their simple availability and wide range of biological effects 68 , Studies have shown that the cardioprotective effects of TPs are closely related to their antioxidant, anti-inflammatory, and blood viscosity-altering characteristics 68 , Here, we have reviewed the relevant literature and summarized ten mechanisms of TPs associated with protection against CVD anti-hypertension, lipid-lowering effects, anti-oxidation, anti-inflammation, anti-proliferation, anti-angiogenesis, anti-AS, recovery of endothelial function, anti-thrombosis, myocardial protective effect ,.

Undoubtedly, TPs can significantly reduce the risk of CVDs by reducing the factors related to CVDs. Hypertension is a major risk factor for CVD and a common disease with a high incidence worldwide that is characterized by elevated arterial pressure At present, there are many drugs that treat hypertension and can effectively lower blood pressure but have large side effects and fluctuate greatly while lowering blood pressure 72 , Therefore, the screening of functional food factors with antihypertensive effects is critical for the prevention and treatment of hypertension.

One of the pathogeneses of hypertension is elevated levels of renin, angiotensin, and aldosterone, and so patients with hypertension will experience high renin in their bodies Aqueous extracts of fermented oolong and black teas strongly inhibit renin In addition, supplementation with white, black and green teas in obese mice prevented the development of hypertension Further analysis revealed that this antihypertensive effect was mainly associated with increased expression of antioxidant enzymes induced by TPs such as gallic acid, xanthine and flavanol In a randomized, double-blind, controlled crossover study, black tea intake increased functionally active circulating angiogenic cells compared to placebo, thereby greatly offsetting the reduction in blood flow-mediated dilation due to fat intake In two epidemiological studies [ATTICA and MEDiterranean ISlands MEDIS ], green tea is rich in high levels of catechins e.

In addition, tannins in tea have been shown to have a hypotensive effect on rats Gao et al. Hyperlipidemia is an important factor that induces CVD. An increase in LDL-C and a decrease in HDL-C in serum can cause arterial endothelial cell damage, increase permeability and accelerate LDL-C deposition in the subendothelium of blood vessels In recent years, a large number of studies have shown that TPs can significantly reduce serum TC, TG, and LDL-C levels and increase HDL-C levels in patients with hyperlipidemia, which can protect vascular endothelial function For example, serum levels of cholesterol, LDL and TG were reduced and HDL was significantly increased in experimental rats fed a high-cholesterol diet after the administration of beverages containing theaflavin and theaflavin In a randomized, controlled trial, ingestion of GTC for 4 consecutive weeks significantly reduced fasting serum TG levels TPs have been widely demonstrated to improve lipid metabolism abnormalities by modulating gut microbial species and functions.

Ma et al. Wang et al. Conversely, excessive intake of TPs reduced their beneficial effects on intestinal health Moreover, TPs were effective in reducing leptin in rat serum and inhibiting fatty acid uptake, thereby improving lipid and antioxidant levels Oxidative stress is present throughout the pathology of AS, and another important effect of TPs is their antioxidant properties Due to the number and structure of phenolic hydroxyl groups, catecholates and theaflavins are excellent electron donors and effective free radical scavengers The inhibition of ROS-producing enzymes by TPs may also enhance their antioxidant effects.

Both catechols and TFs inhibit the expression of inducible NO synthase iNOS. Another physiological source of ROS occurs during the oxidation of hypoxanthine and xanthine to uric acid 87 , This reaction is catalyzed by xanthine oxidase, which has now been shown to be inhibited by catechol and theaflavin.

Several studies have shown that catechol induces a variety of enzymes involved in cellular antioxidant defense mechanisms 87 , 90 , Negishi et al. In endothelial cells, EGCG significantly induced subtilisin oxygenase-1 through activation of AKT and Nrf2, resulting in significant protection against hydroperoxide-regulated oxidative stress 87 , In vitro , TPs ameliorated heat stress injury in cardiomyocytes by upregulating Keap1-Nrf2-ARE signaling to enhance its antioxidant capacity and inducing the expression of heat shock proteins Moreover, in Wistar rats, TPs attenuated the HFD-induced increase in intima-media thickness and significantly inhibited vascular oxidative damage In addition, TPs can inhibit the oxidation of lipoproteins in vivo.

In a clinical study, urinary levels of 4-O-methylglutamic acid were significantly increased after subjects took green and black tea, suggesting that intake of TPs could inhibit LDL oxidation in vivo Besides, in a randomized, placebo-controlled, double-blind, crossover trial, green tea extract was ingested, with EGCG and EGC as the main components.

Both of them rapidly bind LDL particles and reduce the degree of oxidation of LDL, thereby reducing the risk of AS associated with oxidative stress The proliferation and migration of vascular smooth muscle cells VSMCs play key roles in the formation and development of AS, postvalvular restenosis and graft vascular lesions In vivo and in vitro experiments showed that catechols inhibited VSMC proliferation and migration Among catechols, EGC, ECG and EGCG were significantly more effective than catechins and epicatechins in preventing proliferation Kim et al.

Additionally, the antiproliferative effects of TPs include interactions with growth factors involved in the proliferation and migration of VSMCs, such as fibroblast growth factor bFGF 97 , EGCG also significantly inhibits c-Jun nuclear translocation and AP-1 binding activity and reduces iNOS expression Moreover, TPs can interact with the matrix metalloprotein MMP system, which contributes to the migration, proliferation, and neointima formation of VSMCs after vascular injury In a rat model of carotid artery injury, catechins reduced MMP-2 activity by upregulating matrix metalloproteinase MMP -2 and TIMP-2, thereby inhibiting neointimal proliferation and improving vascular remodeling Furthermore, in a carotid artery injury model, EGCG reduced VSMC proliferation by inhibiting extracellular signal-regulated kinase ERK , but c-jun and p38 signaling was not affected Moreover, EGCG was shown to inhibit the expression of apoptosis-related proteins and attenuate apoptosis in VSMCs induced by H 2 O 2 Acute and chronic inflammation plays a key role in the development of CVD , TPs can modulate immune responses and have potential anti-inflammatory activity.

For example, in rats fed an atherosclerotic diet, the administration of 0. A clinical study showed that consistent use of green tea or green tea extract significantly reduced serum amyloid alpha, which is an important CVD risk factor, in obese individuals with metabolic syndrome In another randomized, double-blind trial, long-term black tea consumption reduced platelet activation and lowered plasma CRP levels in healthy men, leading to long-term cardiovascular health maintenance Moreover, in female rats with chronic inflammation, supplementation with TPs suppressed the innate immune response to chronic inflammation, thereby alleviating the development of myocardial fibrosis In the early stages of atherosclerosis, leukocytes adhere to vascular endothelial cells and gradually migrate to the vessel wall.

EGCG significantly reduced the migration of neutrophils to the endothelial cell monolayer by inhibiting chemokine production In vitro experiments revealed that EGCG treatment inhibited TNF-α-induced adhesion of THP-1 cells to human umbilical vein endothelial cells In RAW In obese mice fed a HFD, TPs reduced the serum levels of TNFα, IL-1β and IL-6 by inhibiting the activation of NF- κ B In addition, endothelial cells control vascular tone and permeability and are important for maintaining vascular homeostasis Reddy et al.

In addition to the NF- κ B signaling pathway, TPs improved the species abundance of the intestinal microbiota in the cecum, thereby improving the intestinal inflammatory response Additionally, TPs could increase the expression of intestinal tight junction proteins to maintain the integrity of the intestinal barrier, thereby improving intestinal flora dysbiosis and reducing systemic inflammatory responses in obese mice 28 , The pathophysiological features of the cardiovascular system are characterized by a decrease in protective vasoactive substances in the endothelium, which is called endothelial dysfunction 43 , Numerous studies have shown that TPs improve endothelial cell function, lower blood pressure and have vasodilatory effects — For example, in obese prehypertensive women, short-term daily intake of GTE could improve endothelial function Excessive accumulation of ROS is one of the important causal factors leading to endothelial cell dysfunction and hypertension In bovine carotid artery endothelial cells BCAECs , TPs could inhibit ROS production by reducing nicotinamide adenine dinucleotide phosphate NADPH expression, thereby alleviating angiotensin Ang II-induced endothelial cell hyperpermeability and possibly preventing the development of CVD Moreover, in endothelial cells, TPs can bind endothelial extracellular superoxide dismutase eEC-SOD to inhibit LDL oxidation and thus counteract atherosclerosis Endothelial nitric oxide synthase eNOS is a source of nitric oxide in endothelial cells and plays an important role in maintaining the function of endothelial cells Caveolin-1 Cav-1 is a negative regulator of eNOS that can affect cardiovascular function in multiple ways Liu et al.

In addition, TPs can reduce the expression and secretion of plasminogen activator inhibitor-1 PAI-1 , a regulator that plays a key role in AS and hypertensive disease, in endothelial cells in a time-and dose-dependent manner, contributing to cardiovascular protection A clinical study showed that acute black tea intake could activate NO production in endothelial cells, thereby reducing the risk of CVD Angiogenesis is an important pathological cause of the development of CVD For instance, myocardial infarction MI is mainly associated with partial or complete occlusion of microvessels at the site of the lesion Myocardial ischemia—reperfusion mainly refers to the production of necrotic material by ischemic cells when a patient has a myocardial infarction After revascularization, blood passes through the necrotic myocardium in a short time to create reperfusion damage and increase cellular necrosis, which aggravates the symptoms of infarction and leads to malignant arrhythmias To combat these conditions, restoring blood supply to the infarcted area can reduce cardiac remodeling and improve myocardial function Vascular endothelial growth factor VEGF , a homodimeric vasoactive glycoprotein, is a key regulator of angiogenesis.

VEGF levels are significantly elevated in the serum of patients with different CVDs and are often associated with a poor prognosis A growing number of studies have shown that TPs can protect against CVD by suppressing VEGF-mediated angiogenesis. In HUVECs, EGCG blocks the formation of the vascular endothelial growth factor receptor 2 complex, which in turn inhibits VEGF-mediated angiogenesis , In a high-cholesterol diet male New Zealand White rabbit atherosclerosis model, green tea consumption significantly reduced VEGF expression in foam cells and smooth muscle cells, and it is hypothesized that green tea may slow the progression of atherosclerosis by reducing VEGF-induced angiogenesis EGCG also inhibits angiogenesis by reducing the expression of the angiogenic factor bFGF basic fibroblast growth factor After EGCG pretreatment, endothelial cells could induce the expression of membrane-type-1 matrix metalloproteinase MT1-MMP , which promoted endothelial cell migration, and Cav-1, which caused tube formation, was significantly decreased, suggesting that EGCG inhibits angiogenesis AS is the underlying cause of CVD The development of AS has been associated with multiple molecular mechanisms, including endothelial dysfunction, inflammation, oxidative stress, and dysfunctional lipid metabolism The protective effect of TPs on AS has been widely reported , TPs inhibit oxLDL production and thus IKB kinase IKK -mediated NF- κ B activation in a dose-dependent manner and reduce the production of the proinflammatory cytokine TNF-α In a mouse model of AS, EGCG reduced proinflammatory genes and increased antioxidant protein expression in the mouse aorta, and serum C-reactive protein, monocyte chelator protein-1 and ox-LDL were significantly decreased after EGCG treatment Changes in the gut microbiota are also closely associated with the development of AS Liao et al.

In addition, TPs increased the expression of autophagic markers such as LC3, Beclin1 and p62 in the vascular wall of mice, ameliorated lipid metabolism disorders and inhibited AS plaque formation Platelet activation and subsequent thromboembolism are important pathophysiological mechanisms of ischemic CVD The antithrombotic effect of green tea catechins is achieved mainly through the inhibition of platelet aggregation In addition, GTC did not alter anticoagulant activity but mainly altered antiplatelet activity to exert antithrombotic effects in human platelet aggregation assays induced by ADP, collagen, epinephrine, and the calcium ion polymer A in vitro EGCG has also been shown to stimulate tyrosine phosphorylation of platelet-associated proteins e.

Moreover, Kang et al. Inflammatory and oxidative responses caused by endothelial cell injury play equally important roles in thrombosis A recent study showed that EGCG combined with warfarin significantly reduced thrombus weight in a rat model of deep vein thrombosis Ischemia is an extremely common pathological process in myocardial lesions The protective effect of TPs against myocardial injury may be due to their ability to inhibit oxidative stress associated with ischemic injury For example, in a cardiac hypertrophy model in rats established by abdominal aortic constriction AC , myocardial tissue had increased malondialdehyde MDA levels and decreased superoxide dismutase SOD activity In contrast, after EGCG treatment, the MDA levels in myocardial tissue decreased, and SOD activity increased.

These results suggest that EGCG ameliorates myocardial injury in rats by inhibiting oxidative stress In a rat model of diabetic cardiomyopathy, TPs significantly improved myocardial function in rats, and cardiomyocyte disorders and hypertrophy were significantly improved In addition, ingestion of TPs significantly alleviated heat stress injury in hen cardiomyocytes at 38°C, as evidenced by the downregulation of myocardial injury-related indicators LDH, CK, CK-MB and TNF-α , and the mechanism mainly involved Keap1-Nrf2-ARE and heat shock protein Hsp -related heat stress responses Interestingly, a recent study showed that despite the low plasma concentration of polyphenols, polyphenols were transported to the arterial intima at pH 7.

Thereafter, such high local concentrations of polyphenols protect the heart through direct antioxidant effects In addition, TPs alleviate myocardial fibrosis in female rats by attenuating chronic inflammation and suppressing innate immune responses By modulating these molecular mechanisms, TPs can improve aging-related CVDs.

Figure 1. Molecular mechanism of tea polyphenols TPs to improve aging-related cardiovascular diseases CVDs. Natural substances originating from natural food and plants are of great interest due to their low toxicity, low cost and easy availability.

However, the underlying physiological mechanisms of these substances are not fully understood, especially with respect to the cardiovascular system.

The pathophysiological process of CVD is multifactorial and can be affected by tea components in several processes: anti-hypertension, lipid-lowering effects, anti-oxidation, anti-inflammation, anti-proliferation, anti-angiogenesis, anti-AS, recovery of endothelial function, anti-thrombosis, myocardial protective effect Figure 2.

However, a large number of unresolved issues exist that limit the clinical use of TPs. The debated issues are mainly related to dose, specificity, potency, feasibility and short-or long-term side effects in humans. Although naturally occurring polyphenols are generally considered pharmacologically safe, it is also important to note the presence of deleterious effects of these compounds in the body, which are largely dependent on their distribution in the body and the type of cells on which they act.

In addition, the bioavailability of TPs is relatively low when administered orally, and the effective transport of TPs to target organs is an important issue Moreover, some components of tea polyphenols can also interact with nutrients in the body as well as conventional drugs, which are also potential safety issues To address these issues, animal experiments, large cohort studies and human intervention trials are very necessary in the future.

Figure 2. TPs improve aging related-CVDs in ten ways. CVDs, cardiovascular diseases; EC, - -epicatechin; ECG, - -epicatechingallate; EGC, - -epigallocatechin; EGCG, - -epigallocatechingallate; TPs, tea polyphenols.

In conclusion, a growing body of data suggests that TPs have an important role in the prevention and treatment of CVD by interfering with multiple signal transduction pathways. However, the specific molecular roles of TPs in various cells need to be studied in great depth.

JG, YaL, and YiL wrote the paper. KL collected the references. All authors contributed to the article and approved the submitted version.

This work is supported by funds from the National Natural Science Foundation of China , the Beijing Hospital Nova Project BJ , and the Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences I2M The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Aguilar, VM, Paul, A, Lazarko, D, and Levitan, I.

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J Physiol Biochem Uchida-Maruki H, Inagaki H, Ito R, Kurita I, Sai M, Ito T Piceatannol lowers the blood glucose level in diabetic mice.

Biol Pharm Bull Palmer RM The L-arginine: nitric oxide pathway. Curr Opin Nephrol Hypertens — Wallerath T, Deckert G, Ternes T, Anderson H, Li H, Witte K, Förstermann U Resveratrol, a polyphenolic phytoalexin present in red wine, enhances expression and activity of endothelial nitric oxide synthase.

Li H, Wallerath T, Förstermann U Physiological mechanisms regulating the expression of endothelial-type NO synthase. Nitric Oxide Biol Chem — Kostyuk VA, Potapovich AI, Suhan TO, De Luca C, Korkina LG Antioxidant and signal modulation properties of plant polyphenols in controlling vascular inflammation.

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King RE, Kent KD, Bomser JA Resveratrol reduces oxidation and proliferation of human retinal pigment epithelial cells via extracellular signal-regulated kinase inhibition. Chem Biol Interact Chan CM, Huang CH, Li HJ, Hsiao CY, Su CC, Lee PL, Hung CF Protective effects of resveratrol against UVA-induced damage in ARPE19 cells.

Int J Mol Sci Neal SE, Buehne KL, Besley NA, Yang P, Silinski P, Hong J, Ryde IT, Meyer JN, Jaffe GJ Resveratrol protects against hydroquinone-induced oxidative threat in retinal pigment epithelial cells. Investig Ophthalmol Vis Sci Losa GA Resveratrol modulates apoptosis and oxidation in human blood mononuclear cells.

Eur J Clin Investig Guo R, Su Y, Liu B, Li S, Zhou S, Xu Y Resveratrol suppresses oxidised low-density lipoprotein-induced macrophage apoptosis through inhibition of intracellular reactive oxygen species generation, lox-1, and the p38 MAPK pathway.

Cell Physiol Biochem Olas B, Wachowicz B Resveratrol and vitamin C as antioxidants in blood platelets. Tadolini B, Juliano C, Piu L, Franconi F, Cabrini L Resveratrol inhibition of lipid peroxidation.

Free Radic Res Ahmad KA, Clement MV, Pervaiz S Pro-oxidant activity of low doses of resveratrol inhibits hydrogen peroxide — induced apoptosis. Proc Ann N Y Acad Sci — Amato C Advantage of a micronized flavonoidic fraction Daflon mg in comparison with a nonmicronized diosmin.

Proc Angiol — Maksimović ZV, Maksimović M, Jadranin D, Kuzmanović I, Andonović O Medicamentous treatment of chronic venous insufficiency using semisynthetic diosmin — a prospective study.

Acta Chir Iugosl Download references. Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, India. Department of Biosciences, Shifa Tameer-e-Millat University, Islamabad, Pakistan.

Nano-biotechnology and Translational Knowledge Laboratory, Department of Applied Biology, University of Science and Technology Meghalaya USTM , Techno City, Baridua, Ri-Bhoi, Meghalaya, India. Department of Applied Biology, University of Science and Technology Meghalaya, Ri-Bhoi, India. University Institute of Public Health, Faculty of Allied Health Sciences, The University of Lahore, Lahore, Pakistan.

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Key Laboratory for Wild Plant Resources, Kunming Institute of Botany, Kunming, Yunnan, China. Department of Botany, NSS College Nemmara, Palakkad, Kerala, India. Reprints and permissions. Chopra, H. Role of Polyphenols in Cardiovascular Diseases. In: Arunachalam, K. eds Bioprospecting of Tropical Medicinal Plants.

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Rev Cardiovasc Med —13 PubMed Google Scholar Cassidy A, Mukamal KJ, Liu L, Franz M, Eliassen AH, Rimm EB High anthocyanin intake is associated with a reduced risk of myocardial infarction in young and middle-aged women.

Heart — PubMed PubMed Central Google Scholar Artham SM, Lavie CJ, Milani RV, Ventura HO Obesity and hypertension, heart failure, and coronary heart disease — risk factor, paradox, and recommendations for weight loss.

Ochsner J — PubMed PubMed Central Google Scholar Magyar K, Halmosi R, Palfi A, Feher G, Czopf L, Fulop A, Battyany I, Sumegi B, Toth K, Szabados E Cardioprotection by resveratrol: a human clinical trial in patients with stable coronary artery disease. ab Zbikowska HM, Olas B, Wachowicz B, Krajewski T Response of blood platelets to resveratrol.

x Ou HC, Chou FP, Sheen HM, Lin TM, Yang CH, Huey-Herng Sheu W Resveratrol, a polyphenolic compound in red wine, protects against oxidized LDL-induced cytotoxicity in endothelial cells.

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Proc Ann N Y Acad Sci — CAS Google Scholar Amato C Advantage of a micronized flavonoidic fraction Daflon mg in comparison with a nonmicronized diosmin.

Proc Angiol — CAS Google Scholar Maksimović ZV, Maksimović M, Jadranin D, Kuzmanović I, Andonović O Medicamentous treatment of chronic venous insufficiency using semisynthetic diosmin — a prospective study.

View author publications. Editor information Editors and Affiliations Center for Studies in Stem Cells Cell Therapy and Toxicological Genetics CeTroGen , Graduate Program in Health and Development in the Midwest RegionFaculty of Medicine FAMED Federal University of Mato Grosso do Sul UFMS Campo Grande, Cidade Universitária, Pioneiros, Mato Grosso do Sul, Brazil Karuppusamy Arunachalam Key Laboratory for Wild Plant Resources, Kunming Institute of Botany, Kunming, Yunnan, China Xuefei Yang Department of Botany, NSS College Nemmara, Palakkad, Kerala, India Sreeja Puthanpura Sasidharan.

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