绿茶有效成分表没食子儿茶素没食子酸酯的肿瘤防治作用

表没食子儿茶素食子酸酯（ＥＧＣＧ）是绿茶中最重要的有效成分之一，本文综述ＥＧＣＧ的抑制癌变作用及其主要作用机制，研究表明，ＥＧＣＧ有抗突变、抗促癌、抗氧化以及抑制肿瘤细胞增殖、促进肿瘤细胞凋亡和分化的作用，并影响癌基因的表达等。     

表没食子儿茶素没食子酸酯药理作用研究进展

表没食子儿茶素没食子酸酯是从绿茶中提取分离的一种多酚类单体化合物,是绿茶中儿茶素类化合物的主要组成部分。近年研究发现,其在体内外具有抗肿瘤、抗氧化、抗炎、降血脂、防辐射等多种重要的生物活性。综述了近5年来对表没食子儿茶素没食子酸酯药理作用及作用机制的研究进展。     

表没食子儿茶素没食子酸酯抗肝癌作用机制研究进展

茶的饮用量仅次于水,其保健作用也被世人认可.表没食子儿茶素没食子酸酯[(一)-epigallocatechin-3-gallate,EGCG]是绿茶中含量最高的生物活性成分,其癌症防治作用和细胞作用靶点已被深入研究.本文主要就EGCG的抗肝癌作用机制研究进展综述如下.     

表没食子儿茶素没食子酸酯对大鼠心肌缺血再灌注损伤的保护作用

目的观察表没食子儿茶素没食子酸酯(EGCG)对大鼠心肌缺血再灌注损伤的保护作用。方法结扎左冠状动脉前降支30mm再灌注60m in复制大鼠心肌缺血再灌注模型,实验分假手术组、缺血再灌注组(IR)、EGCG1(10mg·kg^-1)、EGCG2(20mg·kg^-1)和丹参(SM,1.0g·kg^-1)治疗组。用心功能分析系统测定左室心功能,按试剂盒说明测定血浆SOD,MDA,LDH和CK水平,用TUNEL法检测凋亡细胞,SABC免疫组化法检测凋亡相关基因bcl-2与bax的蛋白表达。结果①缺血再灌注期间,IR组大鼠左室LVSP,±dp/dt_max呈进行性下降,LVEDP则进行性升高(与假手术组比,P<0.01),EGCG组虽有相似的变化趋势,但明显较缓(与IR组比,P<0.01)。②IR组大鼠血浆SOD水平显著降低;MDA,LDH与CK水平显著升高。EGCG组SOD水平则明显升高;MDA,LDH与CK水平明显降低(P<0.01)。③IR组心肌凋亡细胞明显,bcl-2与bax蛋白表达增多,bcl-2/bax值下降;EGCG组凋亡细胞减少,bcl-2蛋白表达显著增多,bax则明显减少,bcl-2/bax值升高(P<0.01)。结论EGCG通过提高机体清除自由基能力减轻心肌细胞损伤和抑制心肌细胞凋亡而改善心功能,对大鼠心肌缺血再灌注损伤具有保护作用。     

表没食子儿茶素没食子酸酯对肾缺血再灌注损伤的保护作用

目的　探讨表没食子儿茶素没食子酸酯 (EGCG)对大鼠肾缺血再灌注损伤的影响。方法　通过结扎肾动脉 60min后再灌注 ,建立大鼠肾缺血再灌注损伤模型 ,给药组于结扎前后分别静脉给予 10mg·kg-1和 40mg·kg-1EGCG。化学法观察大鼠血清肌酐 (Scr)、尿素氮 (Bun)、丙二醛(MDA)含量 ,肾组织内MDA、活性氧 (ROS)含量和超氧化物歧化酶 (SOD)、Ca2 + ATP酶活性的变化 ,并观察肾组织的病理变化。结果　与模型对照组比较 ,40mg·kg-1的EGCG组可抑制由肾缺血再灌注引起的血清Bun、Scr、MDA含量和组织MDA、ROS含量的变化 ,增强SOD和Ca2 + ATP酶活性 ,减轻肾组织病理改变。结论　EGCG有保护大鼠肾缺血再灌注损伤的作用 ,其机制可能与抗自由基损伤和减少细胞内钙有关     

表没食子儿茶素没食子酸酯对大鼠心肌缺血再灌注损伤的保护作用

目的观察表没食子儿茶素没食子酸酯(EGCG)对大鼠心肌缺血再灌注损伤的保护作用。方法结扎左冠状动脉前降支30mm再灌注60m in复制大鼠心肌缺血再灌注模型,实验分假手术组、缺血再灌注组(IR)、EGCG1(10mg.kg-1)、EGCG2(20mg.kg-1)和丹参(SM,1.0g.kg-1)治疗组。用心功能分析系统测定左室心功能,按试剂盒说明测定血浆SOD,MDA,LDH和CK水平,用TUNEL法检测凋亡细胞,SABC免疫组化法检测凋亡相关基因bc l-2与bax的蛋白表达。结果①缺血再灌注期间,IR组大鼠左室LVSP,±dp/dtm ax呈进行性下降,LVEDP则进行性升高(与假手术组比,P<0.01),EGCG组虽有相似的变化趋势,但明显较缓(与IR组比,P<0.01)。②IR组大鼠血浆SOD水平显著降低;MDA,LDH与CK水平显著升高。EGCG组SOD水平则明显升高;MDA,LDH与CK水平明显降低(P<0.01)。③IR组心肌凋亡细胞明显,bc l-2与bax蛋白表达增多,bc l-2/bax值下降;EGCG组凋亡细胞减少,bc l-2蛋白表达显著增多,bax则明显减少,bc l-2/bax值升高(P<0.01)。结论EGCG通过提高机体清除自由基能力减轻心肌细胞损伤和抑制心肌细胞凋亡而改善心功能,对大鼠心肌缺血再灌注损伤具有保护作用。     

表没食子儿茶素没食子酸酯抗乳腺癌作用机制的研究进展

乳腺癌是女性最常见的恶性肿瘤，其发病率呈逐年上升趋势。表没食子儿茶素没食子酸酯（EGCG）是茶叶中的主要活性成分之一，具有抗氧化、抗炎症、保护心血管、预防糖尿病及抗肿瘤等功效。近年来，多项体内和体外研究表明EGCG通过抑制细胞增殖、血管生成、干性、侵袭转移及促进凋亡等方式抑制乳腺癌的发生发展。主要对EGCG抑制乳腺癌的分子机制进行综述，为乳腺癌的防治提供新的线索。     

表没食子儿茶素没食子酸酯抗氧化作用机制的研究进展

表没食子儿茶素没食子酸酯(EGCG)是绿茶中的主要儿茶素,大量研究表明绿茶在治疗严重慢性疾病如心血管病、神经退行性病变、肿瘤、代谢综合征、2型糖尿病等方面发挥了积极的生物学作用。绿茶的这种保护性作用主要归因于EGCG强有力的抗氧化活性。EGCG的抗氧化作用机制主要包括清除自由基、金属螯合、抑制细胞信号转导通路、调节氧化和抗氧化酶系等。综述了其抗氧化机制的研究进展,以期为临床应用及开发相同或相似机制的药物提供理论依据。     

表没食子儿茶素没食子酸酯对鱼藤酮诱导PC12细胞损伤的保护作用

目的探讨表没食子儿茶素没食子酸酯(EGCG)对鱼藤酮诱导的嗜铬细胞瘤PC12细胞损伤的保护作用及其可能机制。方法将培养的大鼠PC12细胞分别加入EGCG1,5和10μmol.L-1预处理30 min后加入鱼藤酮250 nmol.L-1继续作用24 h。MTT比色法检测细胞存活率,Hoechst33258染色观察细胞核形态的变化,流式细胞仪检测细胞凋亡率,JC-1染色检测线粒体膜电位变化。结果与鱼藤酮模型组存活率(77.0±1.3)%相比,EGCG1,5和10μmol.L-1组细胞存活率显著增加(P<0.05),分别为(79.8±2.3)%,(82.4±2.2)%和(88.3±2.0)%。Hoechst33258染色发现,EGCG组细胞核形态明显改善。与正常对照组比较,模型组细胞凋亡率增加8.2倍;与鱼藤酮模型组比较,EGCG组细胞凋亡率分别下降46%,25%和63%,差异具有统计学意义(P<0.01)。流式细胞仪检测鱼藤酮组凋亡率为33.8%,EGCG 1,5和10μmo.lL-1组的凋亡率下降至30.6%,14%和15.7%。与模型组相比,EGCG1,5和10μmol.L-1组线粒体膜分别增高了2.48,3.96和4.04倍,差异具有统计学意义(P<0.01)。结论 EGCG具有抑制鱼藤酮诱导的细胞凋亡作用,其机制可能与其稳定线粒体膜电位有关。     

氧化应激致心室重构的研究进展

心室重构意味着血管壁中氧化应激水平的提高,当机体受到有害刺激时,氧化和抗氧化之间失衡,导致大量活性氧簇（ ROS）的产生,加速心室重构的进展。近年来,新型抗氧化剂成为治疗或预防心室重构的靶点,观察抗氧化剂治疗在心室重构患者的长期应用是当下趋势。该文就氧化应激与心室重构之间的关系及相关药物治疗进行综述。     

表没食子儿茶素没食子酸酯对脂多糖诱导原代胶质细胞炎性反应的保护作用

目的:观察表没食子儿茶素没食子酸酯[(-)-Epigallocatechin-3-gallate,EGCG]对细菌脂多糖 (LPS) 所致原代神经胶质细胞炎性反应的保护作用。方法:取新生乳鼠原代神经胶质细胞培养,利用LPS引起其炎症反应。用酶联免疫吸附试验 (ELISA) 测定炎性因子肿瘤坏死因子(TNF-α)、白介素-1β(IL-1β)、白介素-1β(IL-8)表达情况和蛋白免疫印记法(Western blot) 检测炎症因子(诱导型一氧化氮合酶)iNOS蛋白含量变化。结果:LPS激活神经胶质细胞后诱导炎症因子过度表达,大幅上调TNF-α、IL-1β、IL-8炎性因子(P<0.05),iNOS蛋白质水平显著升高(P<0.05),不同浓度EGCG干预组均可明显抑制炎症因子的过度产生,一定程度上减轻LPS诱导神经胶质细胞的炎性反应。结论:一定浓度范围内,EGCG能减弱LPS引起的体外培养神经胶质细胞的炎症反应。     

Excitotoxicity and oxidative damages induced by methylmercury in rat cerebral cortex and the protective effects of tea polyphenols

Methylmercury (MeHg) is a highly neurotoxic environmental pollutant that has a high appetency to the central nervous system. The underlying mechanisms of MeHg‐induced neurotoxicity have not been elucidated clearly until now. Therefore, to explore the mechanisms contribute to MeHg‐induced neurotoxicity, rats were exposed to different dosage of methylmercury chloride (CH₃ClHg) (0, 4, and 12 μmol kg^?1) for 4 weeks to evaluate the neurotoxic effects of MeHg. In addition, considering the antioxidative properties of tea polyphenols (TP), 1 mmol kg^?1 TP was pretreated to observe the possible protective effects on MeHg‐induced neurotoxicity. Then Hg, glutamate (Glu) and glutamine (Gln) levels, glutamine synthetase (GS), phosphate‐activated glutaminase (PAG), Na⁺‐K⁺‐ATPase, and Ca²⁺‐ATPase activities, intracellular Ca²⁺ level were examined, glutathione (GSH), malondialdehyde (MDA), protein sulfhydryl, carbonyl, 8‐hydroxy‐2‐deoxyguanosine (8‐OHdG), and reactive oxygen species (ROS) levels, N‐methyl‐D ‐aspartate receptors (NMDARs) mRNA and protein expressions, apoptosis level and morphological changes in the cerebral cortex were also investigated. Study results showed that compared with those in control, exposure to CH₃ClHg resulted in excitotoxicity in a concentration‐dependent manner, which was shown by the Glu‐Gln cycle disruption and intracellular Ca²⁺ homeostasis disturbance. On the other hand, CH₃ClHg exposure resulted in oxidative damages of brain, which were supported by the significant changes on GSH, MDA, sulfhydryl, carbonyl, 8‐OHdG, and ROS levels. Moreover, apoptosis rate increased obviously and many morphological changes were found after CH₃ClHg exposure. Furthermore, this research indicated that TP pretreatment significantly mitigated the toxic effects of MeHg. In conclusion, findings from this study indicated that exposure to MeHg could induce excitotoxicity and oxidative damage in cerebral cortex while TP might antagonize the MeHg‐induced neurotoxicity. © 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 269–283, 2014.     

人参皂苷保护小鼠精原细胞氧化损伤的研究

目的观察人参皂苷对活性氧引起的小鼠睾丸生殖细胞氧化损伤的保护作用。方法利用体外培养的小鼠精原细胞建立氧化应激模型,通过检测生殖细胞活性、脂质过氧化产物丙二醛(MDA)生成、超氧化物歧化酶(SOD)活性和谷胱甘肽(GSH)水平评价人参皂苷对精原细胞氧化损伤的缓解作用。结果次黄嘌呤/黄嘌呤氧化酶(HX/XO)体系产生的活性氧可引起生殖细胞活性降低、MDA的生成量增加、SOD活性和GSH水平降低,而添加人参皂苷(10mg·L-1)能恢复HX/XO引起的生殖细胞活性、SOD活性和GSH水平的下降以及MDA生成的增加。结论人参皂苷可通过抗氧化作用保护活性氧引起的小鼠精原细胞氧化损伤。     

Protection of multiple antioxidants Chinese herbal medicine on the oxidative stress induced by adriamycin chemotherapy

Adriamycin is an effective anthracycline anti-tumor antibiotic. However, the clinical use of adriamycin has been restricted by its serious side effects. Some reports indicated that the side effects of adriamycin could cause systemic injury, in which reactive oxygen species (ROS) play an important role. ROS are a large family of oxygen free radical and non-free radical active oxygen-containing molecules, including superoxide radical, hydrogen peroxide and hydroxyl radical, which contribute to oxidative stress. Although antioxidant treatment is a promising method to prevent the side effects, protection by a single antioxidant is limited. The Chinese herbal medicine ANTIOXIN is a multiple antioxidant that can effectively block oxidative stress. It was hypothesized that ANTIOXIN could effectively reduce the side effects of adriamycin. A rat tumor model with a transplanted tumor in the liver was treated with adriamycin and ANTIOXIN was used as a protection. Oxidative stress and antioxidant enzymes were evaluated. The results showed that adriamycin chemotherapy increased the level of malondialdehyde (MDA), nitrogen oxide (NO) and decreased the activities of total superoxide dismutase (T-SOD), manganese superoxide dismutase (MnSOD), catalase (CAT), glutathione (GSH) and total antioxidant capacity (TAC). Adriamycin chemotherapy also decreased the expression of Bcl-2, increased the expression of iNOS and cell apoptosis in the liver and kidney. Multiple antioxidants ANTIOXIN had an antagonistic effect on these changes and significantly decreased the mortality of the experimental rats. These data demonstrated that adriamycin chemotherapy could cause oxidative stress to the whole body, on which multiple antioxidants based on the theory of 'multiple antioxidant chain' had effective protection.     

SirT3调节氧化应激作用

依赖于烟酰胺腺嘌呤二核苷酸的去乙酰化酶Sirtuin-3(SirT3)是在进化上高度保守的Sirtuin家族成员之一,能对线粒体内相关的乙酰化蛋白脱乙酰基,通过增加活性氧自由基(ROS)清除酶活性和稳定线粒体功能来抑制线粒体内ROS的蓄积。该文综述了SirT3调节因氧化应激诱发的功能性及器质性损伤的作用和机制,为SirT3在相关病理及生理机制的研究提供有益的参考。     

吡格列酮对培养的心肌细胞肥大的抑制作用

目的利用体外培养的乳鼠心肌细胞,观察吡格列酮对高浓度葡萄糖与去甲肾上腺素共同诱导的肥大心肌细胞的影响,进一步推测吡格列酮对糖尿病性心肌肥大的可能作用及作用机制。方法以培养的乳鼠心肌细胞为模型分组给药后,用显微镜目镜计数心肌细胞搏动的频率;用Lowry’s法测心肌细胞的蛋白质含量;用[3H]leucine标记法测定心肌细胞蛋白的合成;利用计算机图象分析系统测心肌细胞的体积。结果吡格列酮在1～10μmol·L-1浓度对25.5mmol·L-1高糖与1μmol·L-1去甲肾上腺素联合诱导的肥大心肌细胞的蛋白含量、蛋白合成及体积均有显著的抑制作用。其抑制肥大的效果比1μmol·L-1维拉帕米更为显著;同时观察到10μmol·L-1吡格列酮同1μmol·L-1维拉帕米一样有抑制心肌细胞搏动的作用。结论吡格列酮能有效抑制高糖与去甲肾上腺素联合诱导的心肌细胞肥大。这种作用可能是通过作用于PPARγ来实现的。     

Skin delivery of epigallocatechin-3-gallate (EGCG) and hyaluronic acid loaded nano-transfersomes for antioxidant and anti-aging effects in UV radiation induced skin damage

The present work attempts to develop and statistically optimize transfersomes containing EGCG and hyaluronic acid to synergize the UV radiation-protective ability of both compounds, along with imparting antioxidant and anti-aging effects. Transfersomes were prepared by thin film hydration technique, using soy phosphatidylcholine and sodium cholate, combined with high-pressure homogenization. They were characterized with respect to size, polydispersity index, zeta potential, morphology, entrapment efficiency, Fourier Transform Infrared Spectroscopy (FTIR), Differential Scanning Calorimetry (DSC), X-ray Diffraction (XRD), in vitro antioxidant activity and ex vivo skin permeation studies. Cell viability, lipid peroxidation, intracellular ROS levels and expression of MMPs (2 and 9) were determined in human keratinocyte cell lines (HaCaT). The composition of the transfersomes was statistically optimized by Design of Experiments using Box–Behnken design with four factors at three levels. The optimized transfersome formulation showed vesicle size, polydispersity index and zeta potential of 101.2?±?6.0?nm, 0.245?±?0.069 and ?44.8?±?5.24?mV, respectively. FTIR and DSC showed no interaction between EGCG and the selected excipients. XRD results revealed no form conversion of EGCG in its transfersomal form. The optimized transfersomes were found to increase the cell viability and reduce the lipid peroxidation, intracellular ROS and expression of MMPs in HaCaT cells. The optimized transfersomal formulation of EGCG and HA exhibited considerably higher skin permeation and deposition of EGCG than that observed with plain EGCG. The results underline the potential application of the developed transfersomes in sunscreen cream/lotions for improvement of UV radiation-protection along with deriving antioxidant and anti-aging effects.     

Effects of Epigallocatechin-3-gallate on lead-induced oxidative damage

Recent studies have shown that lead (Pb) could disrupt the prooxidant/antioxidant balance of tissue which leads to biochemical and physiological dysfunction. Epigallocatechin-3-gallate (EGCG), a catechin polyphenols component, is found to be an effective antioxidant. The present study investigated whether EGCG administration could reverse the changes on redox states in rat hippocampus caused by lead exposure. The association between redox status changes and long-term potentiation (LTP) in CA1 area of hippocampus were also examined. Wistar rats exposed to lead from postnatal day 1 were followed by 10 days of EGCG (10, 25 and 50 mg/kg) administration through intraperitoneally (ip), and the rats were sacrificed for experiments at the age of 21–23 days. The experimental results showed that glutathione (GSH) and superoxide dismutase (SOD) activity decreased accompanied with LTP amplitude decrease in CA1 area of hippocampus in the lead-exposed group. EGCG supplementation following lead intoxication resulted in increases in the GSH and SOD levels and increases in the LTP amplitude. Malondialdehyde (MDA) levels, a major lipid peroxidation byproduct, increased following lead exposure and decreased following EGCG treatment. In hippocampal neuron culture model, lead exposure (20 μM) significantly inhibited the viability of neurons which was followed by an accumulation of ROS and a decrease of mitochondrial membrane potential (ΔΨ_m). Treatment by EGCG (10–50 μM) effectively increased cell viability, decreased ROS formation and improved ΔΨ_m in hippocampal neurons exposed to lead. These observations suggest that EGCG is a potential complementary agent in the treatment of chronic lead intoxication through its antioxidative character.     

Anti-apoptotic and cytoprotective effect of Enicostemma littorale against oxidative stress in Islets of Langerhans

Context Oxidative stress induces apoptosis within Islets of Langerhans in diabetes mellitus (DM). Enicostemma littorale blume, herb of the Gentianaceae family is used as an anti-diabetic agent across rural India.

Objective This report demonstrates potent anti-apoptotic and cyto-protective activity of Enicostemma littorale MeOH extract (EL MeOH ext.) against 50?μM H₂O₂ in isolated rat Islets.

Materials and methods In this study, the whole plant methanolic extract of EL with doses 0.25–4?mg/mL each for the preincubation duration of 0.5–4?h against 50?μM H₂O₂ were tested for optimum protective dose and time by Trypan blue dye exclusion assay. Islet intracellular reactive oxygen species (ROS) was quantified by DCFDA staining and cell death using PS/PI & FDA/PI staining. Further, comet assay, biochemical assessment of caspase-3 and antioxidant enzyme activities along with immunoblotting of PARP-1, caspase-3, TNF-α activation and p-P38 MapK (stress kinase) induction was performed.

Results The optimized dose of EL MeOH ext. 2?mg/mL for 2?h was used throughout the study, which significantly decreased total Intracellular ROS and cell death. Further, caspase-3 activity, PARP-1 cleavage, p-P38 MapK (stress kinase) activation and TNF-α levels, which had been significantly elevated, were normalized. Antioxidant enzymes like catalase, superoxide dismutase, reduced glutathione and glutathione peroxidase, along with Comet assay, demonstrated that pretreatment with EL MeOH ext. can augment antioxidant enzyme activities and protect from DNA damage.

Discussion and conclusions Significant anti-apoptotic and cyto-protective effects were mediated by EL with Islets of Langerhans subjected to oxidative stress-induced cell death.