Natural tea polyphenol
Tea polyphenols do not have a single specific target but act through multiple mechanisms. They exhibit antioxidant activity by scavenging free radicals and chelating metal ions. They modulate carcinogen metabolism, inhibit cell proliferation, induce apoptosis, and cause cell cycle arrest. Tea polyphenols also inhibit cyclooxygenase-2 (COX-2) induction and exert estrogenic and thyroid hormone-like effects through receptor activation.

Tea polyphenols known as catechins are key components with many biological functions, including anti-inflammatory, antioxidative, and anticarcinogenic effects. These effects are induced by the suppression of several inflammatory factors including nuclear factor-kappa B (NF-kappaB). While these characteristics of catechins have been well documented, actions of catechins as mediators on inflammation-related cardiovascular diseases have not yet been well investigated. In this article, we reviewed recent papers to reveal the anti-inflammatory effects of catechins in cardiovascular diseases. In our laboratory, we performed oral administration of catechins into murine and rat models of cardiac transplantation, myocarditis, myocardial ischemia, and atherosclerosis to reveal the effects of catechins on the inflammation-induced ventricular and arterial remodeling. From our results, catechins are potent agents for the treatment and prevention of inflammation-related cardiovascular diseases because they are critically involved in the suppression of proinflammatory signaling pathways[1].
In vitro, tea polyphenols exhibit anti-carcinogenic, anti-oxidative, anti-allergic, antiviral, anti-hypertensive, anti-atherosclerosis, anti-cardiovascular disease, and anti-hypercholesterolemic activities. They inhibit cell proliferation, induce apoptosis, and cause cell cycle arrest. The compounds also modulate carcinogen metabolism and exhibit potent free radical scavenging activity in various cell-based antioxidant assays.

In diabetic models of diabetes, tea polyphenols (400 mg/(kg√d) in the diet for eight weeks) can lower blood pressure and blood lipids [1]. When there is a chronic cerebral infusion shortage, tea polyphenols (400 mg/(kg√d) in diet) can help with spatial cognition problems [5]. After the forced swim test (FST) and tail suspension test (TST) in mice, tea polyphenols (5–20 mg/kg, most recently, for 7 days) demonstrated resistance comparable to tea polyphenols (100–400 mg/kg daily in the diet). Acetaminophen protects the mouse model from hepatotoxicity by reducing the expression of CYP2E1 and CYP1A2 in mice [7]. Rat model of diabetic cardiomyopathy [1]
In vivo, tea polyphenols have demonstrated health benefits in animal models and human studies. They exhibit anti-carcinogenic effects by inhibiting tumor formation and progression. Their antioxidant properties help reduce oxidative stress and inflammation. Tea polyphenols also show cardiovascular protective effects by reducing blood pressure, improving lipid profiles, and inhibiting atherosclerosis. They are used as dietary supplements for their health-promoting properties.

Tea is the most popular beverage in the world, second only to water. Tea contains an infusion of the leaves from the Camellia sinensis plant rich in polyphenolic compounds known as catechins, the most abundant of which is (-)-EGCG. Although tea has been consumed for centuries, it has only recently been studied extensively as a health-promoting beverage that may act to prevent a number of chronic diseases and cancers. The results of several investigations indicate that green tea consumption may be of modest benefit in reducing the plasma concentration of cholesterol and preventing atherosclerosis. Additionally, the cancer-preventive effects of green tea are widely supported by results from epidemiological, cell culture, animal and clinical studies. In vitro cell culture studies show that tea polyphenols potently induce apoptotic cell death and cell cycle arrest in tumor cells but not in their normal cell counterparts. Green tea polyphenols were shown to affect several biological pathways, including growth factor-mediated pathway, the mitogen-activated protein (MAP) kinase-dependent pathway, and ubiquitin/proteasome degradation pathways. Various animal studies have revealed that treatment with green tea inhibits tumor incidence and multiplicity in different organ sites such as skin, lung, liver, stomach, mammary gland and colon. Recently, phase I and II clinical trials have been conducted to explore the anticancer effects of green tea in humans. A major challenge of cancer prevention is to integrate new molecular findings into clinical practice. Therefore, identification of more molecular targets and biomarkers for tea polyphenols is essential for improving the design of green tea trials and will greatly assist in a better understanding of the mechanisms underlying its anti-cancer activity[2].
In vitro enzyme/receptor binding assays for tea polyphenols measure their antioxidant activity using DPPH radical scavenging, ABTS radical scavenging, or FRAP assays. The compounds' ability to inhibit specific enzymes such as COX-2 or aldose reductase can be assessed using purified enzyme preparations and appropriate substrates. Binding to estrogen and thyroid hormone receptors can be evaluated using radioligand displacement assays.

In vitro cell-based assays for tea polyphenols use various cancer cell lines to assess anti-proliferative and pro-apoptotic effects. Cells are treated with serial dilutions of tea polyphenols, and cell viability is measured using MTT or other assays. Apoptosis is assessed by annexin V staining or caspase activity assays. The compounds' effects on cell cycle progression are evaluated by flow cytometry. Anti-inflammatory activity is assessed by measuring cytokine production in stimulated immune cells.

Animal/Disease Models: Diabetic cardiomyopathy model rats[1]
Doses: 400 mg/(kg∙d)
Route of Administration: in diet for eight weeks
Experimental Results:Lowers serum glucose and blood lipids. Improved myocardial structure and function. Induced autophagy in rats in a high-fat state (Increased level of Beclin-1 and the ratio of LC3-II to LC3-I).

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Methods: Sixty Sprague-Dawley (SD) rats were randomly divided into six groups: a normal control group (NC), an obesity group (OB), a diabetic cardiomyopathy group (DCM), a tea polyphenol group (TP), an obesity tea polyphenol treatment group (OB-TP), and a diabetic cardiomyopathy tea polyphenol treatment group (DCM-TP). After successful modeling, serum glucose, cholesterol, and triglyceride levels were determined; cardiac structure and function were inspected by ultrasonic cardiography; myocardial pathology was examined by staining with hematoxylin-eosin; transmission electron microscopy was used to observe the morphology and quantity of autophagosomes; and expression levels of autophagy-related proteins LC3-II, SQSTM1/p62, and Beclin-1 were determined by Western blotting. Results: Compared to the NC group, the OB group had normal blood glucose and a high level of blood lipids; both blood glucose and lipids were increased in the DCM group; ultrasonic cardiograms showed that the fraction shortening was reduced in the DCM group. However, these were improved significantly in the DCM-TP group. Hematoxylin-eosin staining showed disordered cardiomyocytes and hypertrophy in the DCM group; however, no differences were found among the remaining groups. Transmission electron microscopy revealed that the numbers of autophagosomes in the DCM and OB-TP groups were obviously increased compared to the NC and OB groups; the number of autophagosomes in the DCM-TP group was reduced. Western blotting showed that the expression of LC3-II/I and Beclin-1 increased obviously, whereas the expression of SQSTM1/p62 was decreased in the DCM and OB-TP groups (P<0.05). Conclusions: Tea polyphenols had an effect on diabetic cardiomyopathy in rat cardiac function and may alter the levels of autophagy to improve glucose and lipid metabolism in diabetes.[4]
In vivo animal models for tea polyphenols include mouse models of cancer, where the compounds are administered orally or intraperitoneally, and tumor growth is monitored. Models of cardiovascular disease are used to assess effects on blood pressure, lipid profiles, and atherosclerosis. Inflammatory disease models evaluate the anti-inflammatory effects of tea polyphenols. Pharmacodynamic studies measure antioxidant markers and inflammatory cytokines in treated animals.

Tea polyphenols are orally bioavailable and are absorbed from the gastrointestinal tract. They undergo extensive metabolism in the liver and intestine, with metabolites excreted via urine and feces. The compounds have a molecular formula of C17H19N30 and a molecular weight of 281.36. They are typically stored as a solid at room temperature and are soluble in water and organic solvents.

Tea polyphenols have a favorable safety profile and are generally recognized as safe for consumption. They are used in food products as antioxidants and preservatives. High doses may cause gastrointestinal discomfort. The compounds are not known to be genotoxic or carcinogenic at relevant exposure levels. They are used in cosmetic products as functional additives and in pharmaceutical research for their health-promoting properties.

[1]. Tea polyphenols regulate key mediators on inflammatory cardiovascular diseases. Mediators Inflamm. 2009;2009:494928.

[2]. Tea polyphenols, their biological effects and potential molecular targets. Histol Histopathol. 2008 Apr;23(4):487-96.

[3]. Oxidative stress-induced diseases and tea polyphenols. Oncotarget. 2017 Sep 14;8(46):81649-81661.

[4]. Regulation of autophagy by tea polyphenols in diabetic cardiomyopathy. J Zhejiang Univ Sci B. 2018 May;19(5):333-341.

[5]. Green tea polyphenols inhibit cognitive impairment induced by chronic cerebral hypoperfusion via modulating oxidative stress. J Nutr Biochem. 2010 Aug;21(8):741-8.

[6]. Green tea polyphenols produce antidepressant-like effects in adult mice. Pharmacol Res. 2012 Jan;65(1):74-80.

[7]. Protective effect of tea polyphenols against paracetamol-induced hepatotoxicity in mice is significantly correlated with cytochrome P450 suppression. World J Gastroenterol. 2009 Apr 21;15(15):1829-35.

5,7-Dihydroxy-2-(3,4,5-trihydroxyphenyl)-3,4-dihydro-2H-chromene-3-yl 3,4,5-trihydroxybenzoate is a catechin. It has been reported in tea (Camellia sinensis), rockrose (Cistus salviifolius), and other organisms with relevant data. See also: epigallocatechin gallate (note moved here). Reactive oxides (ROS) are intermediates of normal metabolism and play a crucial role in cell signal transduction. Conversely, excessive accumulation of ROS leads to oxidative stress, which typically causes various cellular damages, including decreased intracellular ATP levels, increased cytoplasmic Ca2+, DNA damage, and dysfunction of the lipid bilayer. These effects ultimately lead to various diseases. Tea polyphenols are widely regarded as an excellent antioxidant. They can exert antioxidant effects by directly scavenging reactive oxides or chelating transition metals, or indirectly by upregulating the activity of antioxidant enzymes. In addition, tea polyphenols also have a strong pro-oxidative capacity, which can directly lead to the generation of reactive oxides and indirectly induce apoptosis and death of cancer cells. The mechanism of its pro-oxidative activity in some diseases is not yet fully understood. This article will explore the dual characteristics of tea polyphenols, namely their antioxidant and pro-oxidative properties, and their role in some human diseases caused by oxidative stress. [3]
Tea Polyphenol (TP98) is a natural product mixture derived from green tea leaves. It is also known as tea tannins or tea catechins. The mixture contains flavanols, anthocyanins, and flavonoids. Tea polyphenols have applications in the food industry for antioxidant and preservative functions, in the pharmaceutical industry for antibacterial, anticancer, and anti-aging effects, and in cosmetic products as functional additives. The compound is used primarily for research purposes.

C22H18O11

458.3717

458.084

84650-60-2

84650-60-2 (Tea polyphenol);84650-60-2 (green tea extract);

1287

Brown to reddish brown solid powder

1.9±0.1 g/cm3

909.1±65.0 °C at 760 mmHg

320.0±27.8 °C

0.0±0.3 mmHg at 25°C

1.857

2.08

8

11

4

33

667

0

O1C2C=C(C=C(C=2CC(C1C1C=C(C(=C(C=1)O)O)O)OC(C1C=C(C(=C(C=1)O)O)O)=O)O)O

WMBWREPUVVBILR-UHFFFAOYSA-N

InChI=1S/C22H18O11/c23-10-5-12(24)11-7-18(33-22(31)9-3-15(27)20(30)16(28)4-9)21(32-17(11)6-10)8-1-13(25)19(29)14(26)2-8/h1-6,18,21,23-30H,7H2

[5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)-3,4-dihydro-2H-chromen-3-yl] 3,4,5-trihydroxybenzoate

84650-60-2; 5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)-3,4-dihydro-2H-chromen-3-yl 3,4,5-trihydroxybenzoate; Tea, ext.; [5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)-3,4-dihydro-2H-chromen-3-yl] 3,4,5-trihydroxybenzoate; 107965-88-8; CHEMBL311663; 5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)-3,4-dihydro-2H-1-benzopyran-3-yl 3,4,5-trihydroxybenzoate; 5,7-Dihydroxy-2-(3,4,5-trihydroxyphenyl)chroman-3-yl 3,4,5-trihydroxybenzoate;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~32.5 mg/mL

Solubility in Formulation 1: ≥ 3.25 mg/mL (Infinity mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 32.5 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 3.25 mg/mL (Infinity mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 32.5 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)