(一)一表没食子儿茶素没食子酸酯对胶原诱导性关节炎小鼠免疫调节机制研究

目的 采用鸡Ⅱ型胶原诱导性关节炎(CIA)小鼠模型,观察(-)-表没食子儿茶素没食子酸酯(EGCG)的治疗作用,并探讨其作用机制.方法 给予CIA小鼠EGCG治疗,以磷酸盐缓冲液(PBS)作为阴性对照,观察各组小鼠发病情况.通过对CIA小鼠关节评分和关节病灶病理学检测[苏木素-伊红(HE)染色] 判断EGCG的疗效;通过,3H-胸腺嘧啶核苷(TdR)掺入实验、流式细胞术及Western-blot方法阐明EGCG的免疫学作用机制.结果 ①EGCG能够改善CIA的关节评分、减少病变关节组织炎性细胞浸润;② EGCG能抑制CIA小鼠C Ⅱ反应性脾细胞的增殖[EGCG组每分钟脉冲数(cpm)值3366±199;PBS组cpm值5342+112,P<0.05]和细胞因子白细胞介素(IL)-17的分泌(EGCG组IL-17阳性细胞数占CD4+T细胞0.41%;PBS组占4.05%);③EGCG能提高CIA小鼠淋巴结细胞中IKB的表达,降低磷酸化IKB蛋白水平的表达.结论 EGCG能显著减轻CIA严重程度.EGCG通过抑制CIA小鼠C Ⅱ反应性脾细胞的增殖和炎症因子IL-17的分泌;以及通过抑制CⅡ反应性淋巴结细胞中IKB的磷酸化,增强IKB的表达从而抑制核因子(NF)-κB的活性来治疗CIA.     

表没食子儿茶素没食子酸酯抗肿瘤侵袭转移相关机制的探讨

目的观察茶多酚的有效成分表没食子儿茶素没食子酸酯（EGCG）对人肝癌细胞侵袭转移的影响及探讨其相关机制。方法用免疫细胞化学检测黏蛋白1的表达、人工重组基底膜侵袭小室及明胶酶谱法观察其对人肝癌细胞株HepG2细胞侵袭转移的影响。结果EGCG能抑制HepG2细胞黏蛋白1的表达，对照组HepG2强阳性细胞数为15个，而EGCG组的强阳性细胞数为1个，差异有统计学意义；EGCG能抑制侵袭基底膜的能力，对照组的侵袭细胞数为（53．2±12．6）个，而EGCG组侵袭细胞数为（8．0±5．1）个，差异有统计学意义。EGCG能抑制MMP-2、MMP-9的分泌。结论EGCG具有明显的抗癌侵袭和转移的作用，其机制可能与黏蛋白1的降低有关。     

Green tea polyphenol epigallocatechin-3-gallate shows therapeutic antioxidative effects in a murine model of colitis

Background and aimsLeukocyte infiltration, up-regulation of proinflammatory cytokines and severe oxidative stress caused by increased amounts of reactive oxygen species are characteristics of inflammatory bowel disease. The catechin (2R,3R)-2-(3,4,5-Trihydroxyphenyl)-3,4-dihydro-1(2H)-benzopyran-3,5,7-triol-3-(3,4,5-trihydroxybenzoate), named epigallocatechin-3-gallate, EGCG, has been demonstrated to exert anti-inflammatory and antioxidative properties, reducing reactive oxygen species in the inflamed tissues. The aim of this study was to evaluate the therapeutic effects of EGCG in a murine model of colitis induced by oral administration of dextran sodium sulfate.MethodsMice received a daily oral administration of 6.9 mg/kg body weight EGCG or Piper nigrum (L.) alkaloid (2E,4E)-5-(1,3-benzodioxol-5-yl)-1-piperidin-1-ylpenta-2,4-dien-1-one, named piperine (2.9 mg/kg body weight) or the combination of the both — piperine was used in this combination to enhance the bioavailability of EGCG.ResultsIn vivo data revealed the combination of EGCG and piperine to significantly reduce the loss of body weight, improve the clinical course and increase overall survival in comparison to untreated groups. The attenuated colitis was associated with less histological damages to the colon and reduction of tissue concentrations of malondialdehyde, the final product of lipid peroxidation. Neutrophils accumulation indicator myeloperoxidase was found to be reduced in colon tissue, while antioxidant enzymes like superoxide dismutase and glutathione peroxidase showed an increased activity. In vitro, the treatment with EGCG plus piperine enhanced the expression of SOD as well as GPO and also reduced the production of proinflammatory cytokines.ConclusionThese data support the concept of anti-inflammatory properties of EGCG being generally beneficial in the DSS-model of colitis, an effect that may be mediated by its strong antioxidative potential.     

表没食子儿茶素没食子酸酯对人胰腺癌细胞株SW1990增殖的影响

目的 探讨表没食子儿茶素没食子酸酯(EGCG)对人胰腺癌细胞株SW1990增殖及细胞凋亡、细胞周期的影响.方法 采用四甲基偶氮唑蓝(MTT)比色法检测不同浓度EGCG(6.25、12.5、25、50、100μg/ml)对体外培养的SW1990细胞增殖的影响;采用流式细胞仪检测EGCG(25μg/ml)对SW1990细胞凋亡及不同浓度的EGCG(0、10、20、30、40、50 μg/ml)对SW1990细胞周期的影响.结果 不同浓度EGCG(0、25、50μg/ml)作用SW1990细胞24 h后,吸光度值(A492)分别为0.46±0.04、0.42±0.04、0.27±0.03,48 h后分别为0.48±0.02、0.31±0.03、0.16±0.02,72 h后分别为0.51±0.01、0.24±0.04、0.14±0.04,EGCG呈浓度及时间依赖性抑制SW1990的增殖(P＜0.01).25 μg/ml EGCG作用于SW1990细胞24、48、72 h后的细胞凋亡率分别为(8.33±1.15)%、(19.77±0.81)%、(29.17±0.75)%,而对照组相应的细胞凋亡率分别为(2.77±0.45)%、(3.20±0.26)%、(3.67±0.35)%,两组差异具有统计学意义(P＜0.01).0、20、50 μg/ml EGCG作用SW1990细胞24 h后,G0/G1期细胞分别占(57.59±0.97)%、(62.99±1.91)%、(68.87±1.88)%,随着EGCG浓度的增加,Go/G1期细胞比例明显增加,而S期和G2/M期细胞比例相应下降(P＜0.01).结论 EGCG能明显抑制SW1990细胞的增殖,其机制可能与其诱导SW1990细胞凋亡及调控细胞周期有关.     

表没食子儿茶素没食子酸酯对高糖环境下内皮细胞氧化应激的影响

目的研究不同剂型表没食子儿茶素没食子酸酯（EGCG）对高糖诱导人脐静脉内皮细胞（HUVEC）氧化应激损伤所引起凋亡的抑制作用及人核因子-κB P65（NF-κB P65）表达的影响。方法从新鲜脐带中分离培养HUVEC。用高糖诱导HUVEC表达NF-κB P65,实验组加入不同浓度的EGCG（12．5、25、50、100、200μmol／L）进行干预,PCR检测NF-κB P65mRNA的表达,AV-PI法检测凋亡细胞。结果高糖可诱导HUVEC凋亡,NF-κB P65表达增高;EGCG可抑制NF-κB P65的表达,降低凋亡指数,具有一定的时效关系、剂量关系。结论EGCG可在一定程度上抑制高糖诱导的氧化应激损伤所致的细胞凋亡。EGCG可能是通过抑制高糖所致的NF-κB增高,从而调控HUVEC细胞凋亡过程,发挥对HUVEC的保护作用。     

CCK-8法检测表没食子儿茶素没食子酸酯对胰腺癌PANC-1细胞增殖的抑制作用

目的 检测表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)对体外培养的人胰腺癌细胞系PANC-1增殖的影响.方法 缺氧条件下体外培养胰腺癌PANC-1细胞,外源性给予不同剂量的EGCG(10、20、40、60、80、100、160 μg/mL)作用细胞不同时间(12、24、48 h),CCK-8法检测不同浓度药物对胰腺癌细胞增殖的影响.结果 EGCG可显著抑制人胰腺癌细胞PANC-1的增殖,其抑制率在药物浓度和时间上呈剂量依赖性和时间依赖性关系;160 μg/mL EGCG作用48 h后,PANC-1细胞的生长抑制率高达(91.03±2.32)%.结论 EGCG对体外缺氧培养的人胰腺癌细胞系PANC-1的增殖有显著抑制作用.     

EGCG和染料木黄酮在肿瘤细胞信号传导中的作用

表没食子儿茶素没食子酸酯(epigallocatechin- 3-gallate,EGCG)和染料木黄酮是两种天然的食物组份,具有多种抗癌功效,其抑制肿瘤发生的途径一直备受关注．两者均可抑制特异的酪氨酸激酶(RTKs)及其相应的下游信号通路 RAS／MAPK和P13K/AKT途径,从而发挥其抗肿瘤作用．近年来,两者在临床研究方面也有较大的开展,但需相关的临床实验研究来确定其最佳剂量、方案、毒性和临床效率,以便达到临床的最优化治疗．     

Suppression of human pancreatic carcinoma cell growth and invasion by epigallocatechin-3-gallate

INTRODUCTION: The consumption of green tea is associated with a lower risk of several types of human carcinomas. A number of studies have focused on the possible mechanisms of cancer prevention by tea extracts, especially polyphenols such as epigallocatechin-3-gallate (EGCG). AIMS AND METHODOLOGY: Green tea-derived EGCG was tested in human pancreatic carcinoma cells. The cells (PANC-1, MIA PaCa-2, and BxPC-3) were treated with different doses of EGCG (0, 25, 50, 100, and 200 micromol/L) for 48 hours in culture medium. Proliferation of pancreatic carcinoma cells was measured by means of the WST-1 colorimetric assay. For the study of cell invasion, the cells were incubated with 100 micromol/L EGCG for 2 hours. Then, the cells were added into the cell insert, coated with Matrigel basement membrane matrix. After incubation at 37 degrees C for 24 hours, the cells that had invaded through the Matrigel were counted visually under the microscope. RESULTS: The growth of all three pancreatic carcinoma cells was significantly suppressed by EGCG treatment in a dose-dependent manner. EGCG treatment caused significant suppression of the invasive ability of pancreatic carcinoma cells PANC-1, MIA PaCa-2, and BxPC-3 but did not affect the cell cycle protein cyclin D1. CONCLUSION: EGCG may be a potent biologic inhibitor of human pancreatic carcinomas, reducing their proliferative and invasive activities.     

EGCG对结肠癌HT-29细胞生长的影响及机制

目的 探讨表没食子儿茶素没食子酸酯(EGCG)对人结肠癌细胞株HT-29生长的影响及可能作用机制.方法 采用不同浓度的EGCG处理HT-29细胞,四唑盐比色试验(MTT)法观察处理后细胞的生长情况;流式细胞术(FCM)检测细胞凋亡情况;Western Blot洁检测表皮生长因子受体(EGFR)、细胞外信号调节激酶(ERK)磷酸化水平的表达.结果 EGCG处理后HT-29细胞生长明显抑制,呈现时间、剂量依赖性;HT-29细胞凋亡率升高;EGFR和ERK的磷酸化水平表达下调.结论 EGCG可明显抑制结肠癌HT-29细胞的生长;其可能机制为下调EGFR和ERK的磷酸化水平,从而干预EGFR-ERK信号转导通路.     

The main green tea polyphenol epigallocatechin-3-gallate counteracts semen-mediated enhancement of HIV infection

Peptide fragments, derived from prostatic acidic phosphatase, are secreted in large amounts into human semen and form amyloid fibrils. These fibrillar structures, termed semen-derived enhancer of virus infection (SEVI), capture HIV virions and direct them to target cells. Thus, SEVI appears to be an important infectivity factor of HIV during sexual transmission. Here, we are able to demonstrate that epigallocatechin-3-gallate (EGCG), the major active constituent of geen tea, targets SEVI for degradation. Furthermore, it is shown that EGCG inhibits SEVI activity and abrogates semen-mediated enhancement of HIV-1 infection in the absence of cellular toxicity. Therefore, EGCG appears to be a promising supplement to antiretroviral microbicides to reduce sexual transmission of HIV-1.     

Partially opposite hemorheological effects of aging and training at middle age

Aging impairs blood rheology while various training protocols improve it. The purpose of this study was to delineate the respective role of aging and endurance training on blood rheology. Thirty-two subjects [16 middle-aged men: 8 cyclists (MAcy) and 8 sedentary men (MAsed) and 16 young men: 8 cyclists (Ycy) and 8 sedentary men (Ysed)] were compared in this study. Results showed higher red blood cell (RBC) rigidity and aggregability (AFFIBIO), lower RBC disaggregability (AFFIBIO) at middle age than at 25 yr, regardless of training status. However there was no age-related difference in whole blood viscosity at either native or corrected hematocrit, plasma viscosity, hematocrit, and Myrenne aggregation indexes M and M1. Training was associated with a reduced hematocrit in middle age subjects but not in 25 yr old ones. We evidenced no effect of training on red cell rigidity (Dintenfass's Tk index), in whole blood viscosity at either native or corrected hematocrit, and plasma viscosity. Thus, regular cycling at middle age maintains a low hematocrit but does not prevent aging-related increase in red cell rigidity and aggregability. Specific effects of cycling among other sports may explain this specific pattern.     

The green tea polyphenol, epigallocatechin-3-gallate, inhibits hepatitis C virus entry

Hepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Current antiviral therapy fails to clear infection in a substantial proportion of cases. Drug development is focused on nonstructural proteins required for RNA replication. Individuals undergoing orthotopic liver transplantation face rapid, universal reinfection of the graft. Therefore, antiviral strategies targeting the early stages of infection are urgently needed for the prevention of HCV infection. In this study, we identified the polyphenol, epigallocatechin-3-gallate (EGCG), as an inhibitor of HCV entry. Green tea catechins, such as EGCG and its derivatives, epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC), have been previously found to exert antiviral and antioncogenic properties. EGCG had no effect on HCV RNA replication, assembly, or release of progeny virions. However, it potently inhibited Cell-culture-derived HCV (HCVcc) entry into hepatoma cell lines as well as primary human hepatocytes. The effect was independent of the HCV genotype, and both infection of cells by extracellular virions and cell-to-cell spread were blocked. Pretreatment of cells with EGCG before HCV inoculation did not reduce HCV infection, whereas the application of EGCG during inoculation strongly inhibited HCV infectivity. Moreover, treatment with EGCG directly during inoculation strongly inhibited HCV infectivity. Expression levels of all known HCV (co-)receptors were unaltered by EGCG. Finally, we showed that EGCG inhibits viral attachment to the cell, thus disrupting the initial step of HCV cell entry. Conclusion: The green tea molecule, EGCG, potently inhibits HCV entry and could be part of an antiviral strategy aimed at the prevention of HCV reinfection after liver transplantation.     

表没食子儿茶素没食子酸酯对人胃癌MGC-803细胞增殖及凋亡的影响

目的观察表没食子儿茶素没食子酸酯(EGCG)对人胃癌MGC-803细胞凋亡的影响,并探讨其机制。方法 MGC-803细胞增殖抑制率测算采用MTT法;EGCG作用后,MGC-803细胞凋亡变化采用AO/EB荧光染色、DNA琼脂糖凝胶电泳及流式细胞术检测,细胞有丝分裂原活化蛋白激酶(MAPK)家族3个主要信号分子JNK、ERK、p38的磷酸化水平用Western blot法检测。结果 EGCG对MGC-803细胞生长具有明显的抑制作用,呈时间和剂量依赖性效应(P均<0.05),并可见明显的细胞凋亡特征。100、200μmol/L的EGCG作用24 h后,其细胞DNA在琼脂糖凝胶上可见特征性的阶梯状条带。50、100、200μmol/L的EGCG作用于MGC-803细胞24 h后,细胞DNA出现明显的亚二倍体峰。EGCG抑制人胃癌MGC-803细胞中ERK的活性,并在一定程度上提高p38和JNK的活性。结论 EGCG可抑制人胃癌MGC-803细胞增殖,并诱导其凋亡。其机制与EGCG抑制MGC-803细胞中ERK活性、提高p38和JNK的活性有关。     

Green tea polyphenol epigallocatechin-3-gallate enhances 5-fluorouracil-induced cell growth inhibition of hepatocellular carcinoma cells

Aim: 5‐Fluorouracil (5‐FU) is one of the most commonly used chemotherapeutic drugs. Resistance to 5‐FU is a major cause of chemotherapy failure in advanced‐stage hepatocellular carcinoma (HCC). Green tea polyphenol Epigallocatechin‐3‐gallate (EGCG) plays a critical role in growth inhibition and apoptotic induction in HCC cell lines. The aim of this study is to investigate whether EGCG can enhance 5‐FU‐induced cell growth inhibition and to explore its potential mechanisms. Methods: 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay was used to evaluate cell growth. Western blotting analysis was performed to detect the proteins expression in Hep3B cells. Small interfering RNA was used to suppress cyclooxygenase‐2 (COX‐2) expression. Furthermore, enzyme linked immunosorbent assay was used to test the prostaglandin E₂ (PGE₂) production in cell cultures. Results: Epigallocatechin‐3‐gallate augmented the anti‐tumor effect of 5‐FU in Hep3B cells. Significant difference was observed between the treated groups and the control group (P < 0.05). EGCG (its concentrations at over 5 µmol/L) combined with 5‐FU presented a synergic effect. Furthermore, the combination of EGCG and 5‐FU abrogated the COX‐2 overexpression and PGE₂ secretion induced by 5‐FU. The upregulation of COX‐2 expression decreased the phosphorylation of Akt (Thr³⁰⁸) expression. These appeared to be followed by the AMPK hyperactivation. Conclusion: Epigallocatechin‐3‐gallate sensitizes HCC cells to 5‐FU antitumor activity, and the combination of EGCG and 5‐FU exhibits synergism in chemo‐resistant cancer cells. The results suggest potential novel therapies for the treatment of advanced‐stage liver cancer.     

Green tea polyphenol epigallocatechin-3-gallate blocks PDGF-induced proliferation and migration of rat pancreatic stellate cells

AIM: To clarify the effects of epigallocatechin-3-gallate (EGCG) on the platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of pancreatic stellate cells (PSCs). METHODS: PSCs were isolated from rat pancreas tissue and used in their culture-activated, myofibroblast-like phenotype. Cell proliferation was assessed by measuring the incorporation of 5-bromo-2'-deoxyuridine. Cell migration was assessed using modified Boyden chambers. Cyclin D1, p21waf1, and p27kip1 expression and phosphorylation of PDGF β-receptor, extracellular signal-regulated kinase, and Akt were examined by Western blotting. Activation of phospha-tidylinositol 3-kinase was examined by kinase assay using phosphatidylinositol as a substrate. Cell cycle was assessed by flow cytometry after staining with propidium iodide. RESULTS: EGCG at non-cytotoxic concentrations inhibited PDGF-induced proliferation and migration. This effect was associated with the inhibition of cell cycle progression beyond the G1 phase, decreased cyclin Dl and increased p27kip1 expression. EGCG inhibited tyrosine phosphorylation of PDGF p-receptor and downstream activation of extracellular signal-regulated kinase and phosphatidylinositol 3-kinase/ Akt pathways. CONCLUSION: EGCG inhibited PDGFBB-induced proliferation and migration of PSCs through the inhibition of PDGFmediated signaling pathways.     

EGCG对乙酸诱导大鼠结肠炎的治疗作用及抗氧化机制

目的:在大鼠结肠炎的模型中,研究表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)的治疗作用及其抗氧化损伤作用的机制.方法:SD大鼠60只,随机分为正常对照组(n=10)、模型安慰剂组(n=20)、EGCG治疗组(n=15)、柳氮磺吡啶(SASP)治疗组(n=15).正常组常规饲养,模型安慰剂组、EGCG组、SASP组80 g/L乙酸造模后分别予以生理盐水2 mL/d、EGCG 50 mg/(kg·d)、SASP0.25 g/(kg·d)灌胃治疗7 d,观察大鼠活动状态,进食量,体质量,大便性状,大便出血情况,计算疾病活动指数(DAI),判断疗效.第8天处死大鼠并进行结肠黏膜损伤指数(CMDI)评分,组织学评级,测定组织一氧化氮自由基(NO)、脂质过氧化产物丙二醛(MDA)以及超氧化物歧化酶(SOD)含量.结果:与模型安慰剂组相比,EGCG显著改善DAI(1.1±0.9 vs 3.9±0.4,P＜0.01)、CMDI(1.5±0.9 vs 3.3±0.6,P＜0.05)和组织学评级(4.6±3.1 vs 9.3±2.8,P＜0.01).与SASP组相比,EGCG显著改善DAI(1.1±0.9 vs 3.0±1.2,P＜0.01)、CMDI(1.5±0.9 vs 2.3±0.9,P＜0.05)和组织学评级(4.6±3.1 vs 7.9±4.0,P＜0.05).与模型安慰剂组相比,EGCG组NO含量显著下降(9.1±5.6 μmol/g vs 15.4±5.0μmol/g,P＜0.05),MDA含量也显著下降(0.9±0.6 μmol/gvs 1.5±0.6 μmol/g,P＜0.05),SOD含量显著提高(3090.6±568.4 nkat/mg vs 1373.6±410.1 nkat/mg,P＜0.05).与SASP组相比,EGCG组SOD含量显著提高(3090.6±568.4 nkat/mg vs 1268.6±431.8 nkat/mg,P＜0.05).结论:EGCG可通过抑制氧化损伤减轻结肠炎症反应,且疗效优于传统药物SASP.     

表没食子儿茶素没食子酸酯增强食管癌细胞对紫杉醇的敏感性

目的观察表没食子儿茶素没食子酸酯(EGCG)体外增强紫杉醇对食管癌Ca Es-17细胞化疗敏感性的作用,探讨可能的作用机制。方法实验分为空白对照组、紫杉醇组(培养液中紫杉醇终浓度为360 nmol/L),EGCG组(培养液中EGCG终浓度为20 mg/L)、联合组(培养液中EGCG终浓度为20 mg/L,紫杉醇浓度为360 nmol/L),各组作用24 h,CCK-8法和细胞克隆形成法检测细胞增殖抑制率和存活率,金氏公式评价二药的协同效果;流式细胞仪检测细胞凋亡率及周期分布;Transwell法检测细胞侵袭力;免疫印迹法检测P21蛋白表达水平。结果 EGCG、紫杉醇均可抑制Ca Es-17细胞增殖、诱导细胞凋亡、降低细胞存活率和侵袭力;减少S期细胞数量、阻断细胞周期于G1期,并能上调P21蛋白表达水平(P<0.05),二药联用上述作用效果更为显著(P<0.01)。结论 EGCG能够增强紫杉醇对食管癌Ca Es-17细胞的化疗敏感性,这种作用部分是通过上调P21蛋白实现的。     

Positive inotropic effects of epigallocatechin-3-gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers

BACKGROUND: There is evidence that the tea catechin epigallocatechin-3-gallate (EGCG) modulates myocardial contractility. However, the underlying mechanisms remain to be determined. AIMS: To study potential signalling pathways involved in EGCG-induced contractile parameters. METHODS AND RESULTS: EGCG increased fractional shortening in rat cardiac myocytes and enhanced intracellular systolic Ca2+ concentrations. In isolated rat hearts, perfusion with EGCG resulted in significant, dose-dependent increase in peak systolic left ventricular pressure, as well as in contraction and relaxation velocities. Heart rate did not change. Inhibition of the beta1-receptor with metoprolol had no influence on the contractile effects of EGCG. Furthermore, levels of cAMP and phosphorylation of phospholamban did not change with EGCG, indicating that the beta-receptor pathway is not involved. The L-type Ca2+ channel inhibitors, nifedipine and gallopamil, failed to modulate EGCG-induced increase in contractility. However, the myocardial effects and intracellular calcium transients stimulated by EGCG were significantly reduced by the antagonist of the Na+/H+ exchanger (NHE) methyl-N-isobutyl amiloride (MIA), and by blocking of the reverse mode of the Na+/Ca2+ exchanger (NCX) by KB-R7943. CONCLUSION: These results indicate that Ca2+-dependent positive inotropic and lusitropic effects of EGCG are mediated in part via activation of the Na+/H+ exchanger and the reverse mode of the Na+/Ca2+ exchanger in the rat myocardium.     

Attenuation of the inflammatory changes and lipid anomalies by epigallocatechin-3-gallate in hypercholesterolemic diet fed aged rats

Epidemiological studies suggest that even in the absence of other risk factors advanced age itself significantly increases cardiovascular morbidity. Age aggravated inflammatory activity further plays a central role in the pathogenesis of atherosclerosis and its complications. EGCG, a major flavonoid present in green tea extract has been proved to be useful in lowering cholesterol levels thereby slowing down the progression of cardiovascular diseases in young animals. Thus, the endeavor of this study was to assess the impact of high-cholesterol diet on aging and vice versa and to exploit the potential of EGCG to combat age-associated hypercholesterolemia and mitigate inflammation. Male albino rats of Wistar strain (3 months-young and 24 months old-aged) were used in this study. Hypercholesterolemia was induced by the diet comprising of the normal rat chow supplemented with 4% cholesterol and 1% cholic acid. EGCG (100 mg/kg body weight/day) was given orally for 30 days. The results revealed abnormally elevated lipid levels, marker enzymes and inflammatory markers in serum of aged hypercholesterolemic rats when compared to young hypercholesterolemic rats, while treatment with EGCG partially reversed these aberrations. The present work demonstrates the inflammatory responses in hypercholesterolemic atherogenesis during aging and further underscores the salubrious role played by the EGCG in attenuating the inflammatory and lipid anomalies.