表没食子儿茶素没食子酸酯抗流感作用的研究进展

茶叶的饮用历史已有千年,其保健功效得到广泛关注。表没食子儿茶素没食子酸酯(EGCG)是茶叶提取物中含量最高、活性最强的单体,研究表明EGCG具有显著的抗流感病毒活性。因其来源丰富、价格低廉、且无耐药,是抗流感药物的有利候选。本文首次针对EGCG的抗流感机制进行综述,全面评价EGCG的抗流感价值,为后续进一步开发EGCG类抗流感药物提供参考。     

表没食子儿茶素没食子酸酯对活性氧的抑制作用

生物体内的活性氧(Reactive oxygen species,ROS)过量引起氧化应激将导致脂质、DNA和蛋白质氧化损伤,从而引发一系列生理和病理反应。绿茶中茶多酚的主要成分表没食子儿茶素没食子酸酯((-)-Epigallocatechin-3-gallate,EGCG)具有强抗氧化性,能有效抑制ROS。本文简要介绍了生物体内ROS的来源和EGCG的特性及其对ROS的抑制作用。通过检测玫瑰红水溶液在光敏化时所产生~1O_2的1 270 nm近红外发光,分析比较了EGCG和迭代钠(NaN_3)对~1O_2发光的淬灭过程,发现EGCG对~1O_2的淬灭效果比NaN_3更好,为EGCG淬灭~1O_2的定量研究提供理论依据。     

表没食子儿茶素没食子酸酯对大鼠胰岛素抵抗的影响

目的研究表没食子儿茶素没食子酸酯（EGCG）对自发性2型糖尿病GK大鼠的胰岛素抵抗的影响及作用机制。方法 自发性2型糖尿病GK大鼠40只,同系健康对照Wistar大鼠10只,大鼠随机分为：正常对照组、2型糖尿病对照组、2型糖尿病低剂量EGCG（50 mg/kg）治疗组、中剂量（100 mg/kg）组、高剂量EGCG（300 mg/kg）组。干预6周后,分别检测葡萄糖耐量试验、胰岛素耐受试验、肝脏GcK、G6P以及PEPCKmRNA表达情况,以及骨骼肌细胞膜GLUT4含量的变化。结果各剂量治疗组的糖耐量均得到明显改善（P〈0.05）,胰岛素耐量在240 min时较模型对照组有明显差异（P〈0.05）。与模型组比较,低剂量和中剂量治疗组均能提高肝脏葡萄糖激酶（GcK）mRNA的表达（P〈0.05）,同时抑制葡萄糖-6-磷酸酶（G6P）和磷酸烯醇式丙酮酸激酶（PEPCK）mRNA的表达（P〈0.05）;高剂量治疗组肝脏三类酶mRNA的表达与模型对照组相比无明显差异。各剂量治疗组GK大鼠的骨骼肌细胞膜GLUT4的含量较模型对照组均具有明显上调（P〈0.05）。结论中低剂量EGCG可以改善GK大鼠胰岛素抵抗,其作用机制可能与抑制肝脏糖异生作用以及骨骼肌GLUT4的转位水平有关,并且EGCG具有代偿胰岛素的作用。     

表没食子儿茶素没食子酸酯(EGCG)的体内外转化及产物活性研究进展

表没食子儿茶素没食子酸酯(EGCC)是绿茶中含量最为丰富、性质最为活泼的儿茶索类物质.体内外转化研究发现,其在体内外可转化为多种产物,其中一些较EGCG具有更高的生物活性.这些研究对于明确茶的保健机理、开发新药具有重要意义.     

表没食子儿茶素没食子酸酯（EGCG）锗（IV）配合物的研究

研究了以绿茶中表没食子儿茶素没食子酸酯(EGCG)为配体制备有机储配合物的反应。结果表明:EGCG[2.00％(w/w)]与Ge(Ⅳ)按摩尔比3:1,在pH6.50～7.00的缓冲溶液中,于40℃恒温水浴中反应30分钟,生成EGCG-Ge(Ⅳ)金属配合物,产物产率61.81％。按等摩尔连续变换法及摩尔比法测定EGCG-Ge(Ⅳ)配合物组成为[EGCG][Ge(Ⅳ)]=2:1(mol/mol),配合物不稳定常数2.570×10~(-11)。在温度≤40℃的中性溶液中,配合物对光的稳定性较好。此外,对配合物的结构进行了红外、紫外及高效液相分析。 茶多酚粗品、EGCG及EGCG-Ge(Ⅳ)配合物对艾氏腹水肿瘤均表现出一定的抗癌效果。     

鲜茶叶中表没食子儿茶素没食子酸酯的高效提取技术研究

采用鲜磨匀浆提取、负压空化混悬组合技术对新鲜老龄茶叶中的没食子酸酯(EGCG)进行了高效提取,并与干燥老龄茶叶的传统提取工艺进行了对比。结果表明：组合工艺的最佳提取条件为新鲜老龄茶叶高温杀青后,再经常温水匀浆萃取,固液比为1:10,匀浆萃取时间为1 min,滤渣再经负压空化混悬固液提取,固液比为1:10,空化时间为15 min,空化提取2次。新鲜老龄茶叶最佳组合工艺的EGCG提取量为502.85 mg,优于传统干燥老龄茶叶工艺。     

表没食子儿茶素没食子酸酯对心力衰竭小鼠心肌损伤的影响

为了评估表没食子儿茶素没食子酸酯(EGCG)对心力衰竭小鼠心肌损伤的保护作用,本研究通过主动脉弓缩窄术建立了心力衰竭的昆明小鼠模型,然后应用EGCG (20 mg/kg)处理小鼠4周。采用苏木精和伊红染色评价心肌组织的病理改变。采用ELISA法检测血清脑钠肽(BNP)、N末端-脑钠肽前体(NT-proBNP)、白细胞介素-1β(IL-1β)、白细胞介素-6 (IL-6)、肿瘤坏死因子-α(TNF-α)、丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的水平,采用Western blotting检测小鼠心肌组织中collagenⅠ、collagenⅢ、Bcl-2、Bax、caspase-3、TGF-β1、Smad3和p-Smad3水平。采用RT-qPCR检测心肌组织中collagenⅠ和collagenⅢ的表达,通过免疫荧光染色检测TGF-β1和p-Smad3的表达。研究显示,EGCG可有效减弱心力衰竭所致细胞坏死、组织肿胀、心肌纤维断裂等病理变化,并且显著降低心力衰竭诊断标志物BNP和NT-proBNP的水平。EGCG可显著降低小鼠心肌组织中的collagenⅠ和collagenⅢ的表达水平。EGCG处理可显著降低TNF-α、IL-1β和IL-6的水平。EGCG处理显著降低了心力衰竭小鼠血清MDA水平,而升高了SOD和GSH-Px水平。EGCG可显著上调心力衰竭小鼠心肌组织中Bcl2的表达,而下调Bax和caspase-3的表达。TGF-β信号通路激活剂可显著上调心肌组织中的TGF-β表达,而EGCG处理可显著抑制TGF-β1和p-Smad3蛋白的表达。表明EGCG可抑制心力衰竭小鼠的心肌纤维化、炎症反应、氧化应激和细胞凋亡,从而减轻心肌损伤。EGCG对心肌的保护作用可能与抑制TGF-β1/smad3信号通路有关。     

转录激活因子5参与表没食子儿茶素没食子酸酯诱导的胰腺癌SW1990细胞凋亡

目的:研究转录激活因子5(ATF5)是否参与中国绿茶有效成分——表没食子儿茶素没食子酸酯(EGCG)诱导的人胰腺癌SW1990细胞凋亡。方法:采用噻唑蓝(MTT)比色法检测不同浓度的EGCG作用SW1990细胞不同时间后细胞的增殖情况;以100 mg/L EGCG作用SW1990细胞不同时间,观察细胞的形态学变化,并采用SR-VAD-FMK/7-AAD双染法,流式细胞仪检测细胞凋亡情况;采用RT-PCR检测100 mg/L EGCG作用不同时间后ATF5mRNA的表达变化。结果:EGCG可抑制胰腺癌SW1990细胞增殖,引起细胞皱缩,诱导细胞凋亡。随着EGCG作用时间的延长,细胞凋亡率显著提高(P<0.05),ATF5 mRNA的表达明显增强(P<0.05)。结论:胰腺癌SW1990细胞中存在ATF5的表达,在EGCG诱导的细胞凋亡过程中,ATF5表达量上升,提示ATF5参与EGCG诱导的细胞凋亡。     

表没食子儿茶素没食子酸酯对人结肠癌HT-29细胞G1期的阻滞作用

目的:研究表没食子儿茶素没食子酸酯(Epigallaocatechin-3-gallate,EGCG)时人结肠癌HT-29细胞增殖的影响.方法:实验分为EGCG不同浓度处理组和阴性对照组.采用MTT比色法检测EGCG(30μg/mL、40μg/mL、50μg/mL、60μg/mL、70μg/mL)对HT-29细胞的生长影响;应用流式细胞术分析EGCG对HT-29细胞周期分布的影响;免疫印迹观测EGCG对HT-29细胞p38MAPK、cyclinD1蛋白表达的影响.结果:MTT比色结果显示.不同浓度EGCG(30μg/ml、40μg/ml、50μg/ml、60μg/ml)对HT-29细胞具有明显的生长抑制作用,并呈剂量-效应依赖关系(P<0.05);流式细胞术分析显示,EGCG诱导人结肠癌细胞G1期阻滞,且随着处理时间的延长,其诱导周期阻滞的效应越明显(P<0.05);蛋白免疫印迹显示.总的p38MAPK不随处理时间和浓度的改变而改变,但是磷酸化的p38MAPK蛋白的表达随处理时间和处理浓度的增加而明显增加,而CyclinD1蛋白的表达随处理浓度的增加而明显减少.结论:EGCG诱导HT-29细胞G1期阻滞,抑制细胞增殖,可能与活化p38MAPK,下调CyclinD1蛋白表达有关.     

表没食子儿茶素没食子酸酯衍生物及过硫酸氢钾复合物粉体外抑制Ⅰ型草鱼呼肠孤病毒的研究

【目的】为了将表没食子儿茶素没食子酸酯(epigallocatechin gallate, EGCG)的2种衍生物和过硫酸氢钾复合物粉(compound potassium peroxymonosulfate powder, KMPS)运用于体外细胞实验中,以评估这3种药物对I型草鱼呼肠孤病毒(grass carp reovirus, GCRV)的抑制和杀灭效果。【方法】利用MUSE法和CCK-8法评估表没食子儿茶素没食子酸酯棕榈酸酯(epigallocatechin gallate palmitate,EGCG-P)、乙酰化表没食子儿茶素没食子酸酯(peracetylated epigallocatechin gallate, Ac EGCG)和过硫酸氢钾复合物粉3种药物对细胞的安全浓度,利用体外细胞感染病毒模型,使用不同浓度测试物处理病毒或细胞后感染病毒,通过实时荧光定量聚合酶链反应(quantitative real-time polymerase chain reaction, q RT-PCR)法分析不同测试物对病毒的抑制和杀灭效果。使用不同浓度测试物处理细胞后,利用q RT...     

EGCG防治神经退行性疾病的作用机制

表没食子儿茶素没食子酸酯（epigallocatechin-3-gallate,EGCG）是绿茶多酚成分中的一种主要组分,参与了神经细胞生长与凋亡的调控,研究发现其机制可能与抗氧化损伤和影响MAPK．PKC和PI-3K／Akt等细胞内信号转导通路相关。因此,探讨EGCG的神经保护作用及其机制,将为应用EGCG防治帕金森氏症、阿尔茨海默病等中枢神经系统退行性疾病的基础与临床研究提供理论依据。     

Epigallocatechin-3-gallate protects motor neurons and regulates glutamate level

Epigallocatechin-3-gallate (EGCG) is a major component of green tea polyphenols which displays potential properties of anticancer and neuroprotection. Here we show that protection of motor neuron by EGCG is associated with regulating glutamate level in organotypic culture of rat spinal cord. In this model, EGCG blocked glutamate excitotoxicity caused by threohydroxyaspartate, an inhibitor of glutamate transporter. This property of EGCG may be not due to its intrinsic antioxidative activity, because another antioxidant could not regulate glutamate level under the same condition. These results show that EGCG may be a potential therapeutic candidate for neurodegenerative diseases involving glutamate excitotoxicity such as ALS.     

茶树表没食子儿茶素-3-O-(3-O-甲基)没食子酸酯研究进展

表没食子儿茶素-3-O-(3-O-甲基)没食子酸酯(EGCG3"Me)是茶叶中最常检测到的甲基化表没食子儿茶素没食子酸酯(EGCG"Me),具有较表没食子儿茶素没食子酸酯(EGCG)更好的保健功效。本文对EGCG3"Me的理化性质、制备方法、保健功效、茶树EGCG3"Me含量影响因素、EGCG3"Me体内合成路径等国内外研究现状进行了综述,展望EGCG3"Me的体内代谢途径及其深加工产品研发将成为研究热点。     

Epigallocatechin-3-gallate inhibits bacterial virulence and invasion of host cells

Increasing antibiotic resistance and beneficial effects of host microbiota has motivated the search for anti-infective agents that attenuate bacterial virulence rather than growth. For example, we discovered that specific flavonoids such as baicalein and quercetin from traditional medicinal plant extracts could attenuate Salmonella enterica serovar Typhimurium type III protein secretion and invasion of host cells. Here, we show epigallocatechin-3-gallate from green tea extracts also inhibits the activity of S. Typhimurium type III protein effectors and significantly reduces bacterial invasion into host cells. These results reveal additional dietary plant metabolites that can attenuate bacterial virulence and infection of host cells.     

Epigallocatechin-3-gallate (EGCG): chemical and biomedical perspectives

The compound (-)-epigallocatechin-3-gallate (EGCG) is the major catechin found in green tea [Camellia sinensis L. Ktze. (Theaceae)]. This polyphenolic compound and several related catechins are believed to be responsible for the health benefits associated with the consumption of green tea. The potential health benefits ascribed to green tea and EGCG include antioxidant effects, cancer chemoprevention, improving cardiovascular health, enhancing weight loss, protecting the skin from the damage caused by ionizing radiation, and others. The compound EGCG has been shown to regulate dozens of disease-specific molecular targets. Many of these molecular targets are only affected by concentrations of EGCG that are far above the levels achieved by either drinking green tea or consuming moderate doses of green tea extract-based dietary supplements. In spite of this, well-designed double-blinded controlled clinical studies have recently demonstrated the efficacy of green tea extracts and purified EGCG products in patients. Therefore, this review highlights results from what the authors believe to be some of the most clinically significant recent studies and describes current developments in the stereoselective total synthesis of EGCG.     

Epigallocatechin-3-gallate potently inhibits the in vitro activity of hydroxy-3-methyl-glutaryl-CoA reductase

Hydroxy-3-methyl-glutaryl-CoA reductase (HMGR) is the rate-controlling enzyme of cholesterol synthesis, and owing to its biological and pharmacological relevance, researchers have investigated several compounds capable of modulating its activity with the hope of developing new hypocholesterolemic drugs. In particular, polyphenol-rich extracts were extensively tested for their cholesterol-lowering effect as alternatives, or adjuvants, to the conventional statin therapies, but a full understanding of the mechanism of their action has yet to be reached. Our work reports on a detailed kinetic and equilibrium study on the modulation of HMGR by the most-abundant catechin in green tea, epigallocatechin-3-gallate (EGCG). Using a concerted approach involving spectrophotometric, optical biosensor, and chromatographic analyses, molecular docking, and site-directed mutagenesis on the cofactor site of HMGR, we have demonstrated that EGCG potently inhibits the in vitro activity of HMGR (K(i) in the nanomolar range) by competitively binding to the cofactor site of the reductase. Finally, we evaluated the effect of combined EGCG-statin administration.     

商陆不同极性、根和茎提取物的抑菌性能分析

为探究商陆不同极性、部位提取物的抑菌性能,本实验分别从商陆根和茎中提取石油醚相、乙酸乙酯相、正丁醇相和水相4种不同极性的提取物,再采用滤纸片法测量提取物对大肠杆菌(Escherichia coli)、金黄色葡萄球菌(Staphyloccocus aureus)、巨大芽孢杆菌(Bacillus megaterium)和副溶血弧菌(Vibrio parahaemolyt-icus)4种细菌的抑制性能。结果表明,部分商陆的提取物有一定的抑菌活性,如根正丁醇相对巨大芽孢杆菌和副溶血弧菌,茎水相对副溶血弧菌的抑菌圈在10mm以上,但总体上商陆的提取物的抑菌性能远不及头孢氨苄好。实验还发现商陆抑菌活性最强的物质大都存在于根中,且抑菌活性最强的物质大都存在于水和正丁醇这种极性较高的溶剂的提取物中,不同提取物对不同细菌的抑菌活性情况不一致。因此本研究结果可以为商陆提取物抑菌性能的进一步探索提供参考。     

Epigallocatechin-3-gallate suppresses the global interleukin-1beta-induced inflammatory response in human chondrocytes

Introduction  

Epigallocatechin-3-gallate (EGCG) is a bioactive polyphenol of green tea and exerts potent anti-inflammatory effects by inhibiting signaling events and gene expression. Interleukin-1beta (IL-1β) is the principal cytokine linked to cartilage degradation in osteoarthritis (OA). The objective of this study was to evaluate the global effect of EGCG on IL-1β-induced expression of proteins associated with OA pathogenesis in human chondrocytes.     

Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties

Neuroinflammation has been known to play a critical role in the pathogenesis of Alzheimer's disease (AD) through amyloidogenesis. In a previous study, we found that systemic inflammation by intraperitoneal (ip) injection of lipopolysaccharide (LPS) induces neuroinflammation and triggers memory impairment. In this present study, we investigated the inhibitory effects of epigallocatechin-3-gallate (EGCG) on the systemic inflammation-induced neuroinflammation and amyloidogenesis as well as memory impairment. ICR mice were orally administered with EGCG (1.5 and 3 mg/kg) for 3 weeks, and then the mice were treated by ip injection of LPS (250 μg/kg) for 7 days. We found that treatment of LPS induced memory-deficiency-like behavior and that EGCG treatment prevented LPS-induced memory impairment and apoptotic neuronal cell death. EGCG also suppressed LPS-induced increase of the amyloid beta-peptide level and the expression of the amyloid precursor protein (APP), β-site APP cleaving enzyme 1 and its product C99. In addition, we found that EGCG prevented LPS-induced activation of astrocytes and elevation of cytokines including tumor necrosis factor-α, interleukin (IL)-1β, macrophage colony-stimulating factor, soluble intercellular adhesion molecule-1 and IL-16, and the increase of inflammatory proteins, such as inducible nitric oxide synthase and cyclooxygenase-2, which are known factors responsible for not only activation of astrocytes but also amyloidogenesis. In the cultured astrocytes, EGCG also inhibited LPS-induced cytokine release and amyloidogenesis. Thus, this study shows that EGCG prevents memory impairment as well as amyloidogenesis via inhibition of neuroinflammatory-related cytokines released from astrocytes and suggests that EGCG might be a useful intervention for neuroinflammation-associated AD.