Theaflavin(Synonyms: 茶黄素) 目录号 : GC32090
Theaflavin (TF) is a distinctive derivative of benzotropolones first extracted from black tea, and has antioxidant effects for its functions of radical scavenging and metal chelation [1,2].
Sample solution is provided at 25 µL, 10mM.
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|Cell experiment :|
HK-2 cells were treated with or without Theaflavin (20 and 50 µg/ml) for 2 h followed by incubation with 100 mg/ml of calcium oxalate( CaOx ) monohydrate for 24 h.
20 and 50 µg/ml Theaflavin;2 h
Theaflavin inhibited calcium oxalate monohydrate (COM)-induced renal HK-2 tubular epithelial cell oxidative stress injury.
|Animal experiment :|
C57BL/6J mice(CaOx nephrocalcinosis model )
Mice were daily treated with TF by gavage at three different doses (20, 50, and 100 mg/kg) on days 1-14.
20、50、100 mg/kg Theaflavin;14days;i. g.
Theaflavin alleviated CaOx nephrocalcinosis-induced oxidative stress injury and crystal deposition in mice.
.Ye T, Yang X, et,al.Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1. Int J Biol Sci. 2021 Mar 2;17(4):1050-1060. doi: 10.7150/ijbs.57160. PMID: 33867828; PMCID: PMC8040307.
Theaflavin (TF) is a distinctive derivative of benzotropolones first extracted from black tea, and has antioxidant effects for its functions of radical scavenging and metal chelation [1,2]. Besides,theaflavin is a suitable natural inhibitor against influenza A (H1N1) neuraminidase.
Theaflavin(20 and 50 µg/ml;2 h) inhibited calcium oxalate monohydrate (COM)-induced renal HK-2 tubular epithelial cell oxidative stress injury. Human umbilical vein endothelial cells (HUVECs) exposed to Theaflavin(0-200µM;24 h) can alleviate apoptosis and cell dysfunction induced by tert-butyl hydroperoxide (TBHP). Theaflavin(0-160µM;72 h) inhibited proliferation of CNE2 cells, promoted apoptosis, and up-regulated the expression of caspase 3, caspase 9, and Bax, and decreased the level of Bcl-2.
Theaflavin(20、50、100 mg/kg;14days;i. g.) alleviated CaOx nephrocalcinosis-induced oxidative stress injury and crystal deposition in mice. In a renal ischemia/reperfusion(I/R) injury mouse model, theaflavin pretreatment(20/50/80 mg/kg;3days;i. g.) significantly inhibited I/R-induced kidney injury and cell apoptosis. It improved mitochondrial dysfunction by reducing mitochondrial damage and promoting mitochondrial membrane potential.
茶黄素(20和50 µg/ml;2 h)可抑制草酸钙(COM)诱导的肾HK-2小管上皮细胞氧化应激损伤。人脐静脉内皮细胞(HUVECs)暴露于茶黄素(0-200µM;24 h)可减轻过氧化叔丁基(TBHP)诱导的细胞凋亡和功能障碍。茶黄素(0 ~ 160µ m;72 h)抑制CNE2细胞增殖,促进凋亡,上调caspase 3、caspase 9、Bax表达,降低Bcl-2水平。
茶黄素(20、50、100 mg/kg;14days;i. g.)减轻CaOx肾钙质沉着引起的小鼠氧化应激损伤和晶体沉积。在肾缺血再灌注(I/R)损伤小鼠模型中,茶黄素预处理(20/50/80 mg/kg;3days;i. g.)显著抑制了肾损伤和细胞凋亡。它通过减少线粒体损伤和促进线粒体膜电位改善线粒体功能障碍。
. Han X, Zhang J, et al. Theaflavin ameliorates ionizing radiation-induced hematopoietic injury via the NRF2 pathway. Free Radic Biol Med. 2017;113:59-70
. San Cheang W, Yuen Ngai C, et al. Black tea protects against hypertension-associated endothelial dysfunction through alleviation of endoplasmic reticulum stress. Sci Rep. 2015;5:10340
. Sahoo M, Jena L, et,al. Identification of Suitable Natural Inhibitor against Influenza A (H1N1) Neuraminidase Protein by Molecular Docking. Genomics Inform. 2016 Sep;14(3):96-103. doi: 10.5808/GI.2016.14.3.96. Epub 2016 Sep 30. PMID: 27729839; PMCID: PMC5056903.
. Ye T, Yang X, et,al.Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1. Int J Biol Sci. 2021 Mar 2;17(4):1050-1060. doi: 10.7150/ijbs.57160. PMID: 33867828; PMCID: PMC8040307.
. Chen D, Wu Z, et,al.Theaflavin Attenuates TBHP-Induced Endothelial Cells Oxidative Stress by Activating PI3K/AKT/Nrf2 and Accelerates Wound Healing in Rats. Front Bioeng Biotechnol. 2022 Mar 2;10:830574. doi: 10.3389/fbioe.2022.830574. PMID: 35309982; PMCID: PMC8924520.
. Xu J, Wang SJ, et,al.Theaflavin promoted apoptosis in nasopharyngeal carcinoma unexpectedly via inducing autophagy in vitro. Iran J Basic Med Sci. 2022 Jan;25(1):68-74. doi: 10.22038/IJBMS.2021.59190.13143. PMID: 35656444; PMCID: PMC9118283.
. Li Z, Zhu J, et,al. Theaflavin ameliorates renal ischemia/reperfusion injury by activating the Nrf2 signalling pathway in vivo and in vitro. Biomed Pharmacother. 2021 Feb;134:111097. doi: 10.1016/j.biopha.2020.111097. Epub 2020 Dec 16. PMID: 33341051.
|溶解度||Water : 2 mg/mL (3.54 mM);DMSO : 1.42 mg/mL (2.52 mM)||储存条件||Store at -20°C|
|General tips||For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.|
|Shipping Condition||Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
|1 mg||5 mg||10 mg|
|1 mM||1.7715 mL||8.8576 mL||17.7151 mL|
|5 mM||0.3543 mL||1.7715 mL||3.543 mL|
|10 mM||0.1772 mL||0.8858 mL||1.7715 mL|
|% DMSO % % Tween 80 % saline|
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
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Theaflavin Chemistry and Its Health Benefits
Oxid Med Cell Longev 2021 Nov 18;2021:6256618.PMID:34804369DOI:10.1155/2021/6256618.
Huge epidemiological and clinical studies have confirmed that black tea is a rich source of health-promoting ingredients, such as catechins and theaflavins (TFs). Furthermore, TF derivatives mainly include Theaflavin (TF1), theaflavin-3-gallate (TF2A), theaflavin-3'-gallate (TF2B), and theaflavin-3,3'-digallate (TF3). All of these TFs exhibit extensive usages in pharmaceutics, foods, and traditional medication systems. Various indepth studies reported that how TFs modulates health effects in cellular and molecular mechanisms. The available literature regarding the pharmacological activities of TFs has revealed that TF3 has remarkable anti-inflammatory, antioxidant, anticancer, antiobesity, antiosteoporotic, and antimicrobial properties, thus posing significant effects on human health. The current manuscript summarizes both the chemistry and various pharmacological effects of TFs on human health, lifestyle or aging associated diseases, and populations of gut microbiota. Furthermore, the biological potential of TFs has also been focused to provide a deeper understanding of its mechanism of action.
Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1
Int J Biol Sci 2021 Mar 2;17(4):1050-1060.PMID:33867828DOI:10.7150/ijbs.57160.
Renal tubular cell injury induced by calcium oxalate (CaOx) is a critical initial stage of kidney stone formation. Theaflavin (TF) has been known for its strong antioxidative capacity; however, the effect and molecular mechanism of TF against oxidative stress and injury caused by CaOx crystal exposure in kidneys remains unknown. To explore the potential function of TF on renal crystal deposition and its underlying mechanisms, experiments were conducted using a CaOx nephrocalcinosis mouse model established by glyoxylate intraperitoneal injection, and HK-2 cells were subjected to calcium oxalate monohydrate (COM) crystals, with or without the treatment of TF. We discovered that TF treatment remarkably protected against CaOx-induced kidney oxidative stress injury and reduced crystal deposition. Additionally, miR-128-3p expression was decreased and negatively correlated with SIRT1 level in mouse CaOx nephrocalcinosis model following TF treatment. Moreover, TF suppressed miR-128-3p expression and further abolished its inhibition on SIRT1 to attenuate oxidative stress in vitro. Mechanistically, TF interacted with miR-128-3p and suppressed its expression. In addition, miR-128-3p inhibited SIRT1 expression by directly binding its 3'-untranslated region (UTR). Furthermore, miR-128-3p activation partially reversed the acceerative effect of TF on SIRT1 expression. Taken together, TF exhibits a strong nephroprotective ability to suppress CaOx-induced kidney damage through the recovery of the antioxidant defense system regulated by miR-128-3p/SIRT1 axis. These findings provide novel insights for the prevention and treatment of renal calculus.
Theaflavin: a natural candidate to restrain thrombosis
Food Funct 2022 Jul 18;13(14):7572-7581.PMID:35815842DOI:10.1039/d2fo00152g.
Many clinical studies have demonstrated the beneficial effects of black tea on cardiovascular diseases. However, the antiplatelet and antithrombotic activities of Theaflavin (TF-1) remain unknown. In this study, we aimed to investigate the beneficial effects of TF-1 on platelet activation and thrombosis formation both in vitro and in vivo. Firstly, the in vitro antiplatelet activity of TF-1 was analyzed using platelets isolated from human blood via aggregometry, flow cytometry, the ELISA kit, western blot and fluorescence microscopy. Subsequently, the in vivo analysis of the hemostatic state and thrombosis formation was carried out in C57BL/6 mice based on the tail bleeding time and an FeCl3-induced arterial thrombus model. The results showed that TF-1 could prominently inhibit platelet aggregation in a dose-dependent manner, and attenuate P-selectin expression, fibrinogen binding, spreading and thromboxane A2 (TxA2) formation. Western blot analysis showed that TF-1 potently inhibited spleen tyrosine kinase (Syk) and Akt (ser473/474) phosphorylation. The in vivo data further confirmed the inhibition of platelet activation by TF-1 with a prolonged arterial occlusion time (from 15.0 ± 1.1 minutes to 40.0 ± 5.4 minutes). All the results indicated that TF-1 is a powerful inhibitor of platelet activation and thrombosis formation in C57BL/6 mice, and could be developed as a novel food-based inhibitor of thrombotic disorders.
Theaflavin Alleviates Inflammatory Response and Brain Injury Induced by Cerebral Hemorrhage via Inhibiting the Nuclear Transcription Factor Kappa β-Related Pathway in Rats [Retraction]
Drug Des Devel Ther 2022 Jul 20;16:2341-2342.PMID:35899234DOI:10.2147/DDDT.S382792.
[This retracts the article DOI: 10.2147/DDDT.S164324.].
Theaflavin 3-gallate inhibits the main protease (Mpro) of SARS-CoV-2 and reduces its count in vitro
Sci Rep 2022 Jul 30;12(1):13146.PMID:35908093DOI:10.1038/s41598-022-17558-5.
The main protease (Mpro) of SARS-CoV-2 has been recognized as an attractive drug target because of its central role in viral replication. Our previous preliminary molecular docking studies showed that Theaflavin 3-gallate (a natural bioactive molecule derived from Theaflavin and found in high abundance in black tea) exhibited better docking scores than repurposed drugs (Atazanavir, Darunavir, Lopinavir). In this study, conventional and steered MD-simulations analyses revealed stronger interactions of Theaflavin 3-gallate with the active site residues of Mpro than Theaflavin and a standard molecule GC373 (a known inhibitor of Mpro and novel broad-spectrum anti-viral agent). Theaflavin 3-gallate inhibited Mpro protein of SARS-CoV-2 with an IC50 value of 18.48 ± 1.29 μM. Treatment of SARS-CoV-2 (Indian/a3i clade/2020 isolate) with 200 μM of Theaflavin 3-gallate in vitro using Vero cells and quantifying viral transcripts demonstrated reduction of viral count by 75% (viral particles reduced from Log106.7 to Log106.1). Overall, our findings suggest that Theaflavin 3-gallate effectively targets the Mpro thus limiting the replication of the SARS-CoV-2 virus in vitro.