茶多酚的抗氧化和抑菌活性及其增效剂

论述了茶多酚的抗氧化和抑菌活性机理,其中起重要作用的是茶多酚分子内的多个酚羟基。在抗氧化过程中,其酚羟基具有供氢体的活性,阻断自由基的链式反应。在抑菌过程中,其酚羟基可与蛋白质分子中的氨基或羧基结合,其疏水性的苯环结构也可与蛋白质发生疏水结合,茶多酚与蛋白质之间的这种多点结合作用阻止了细菌的侵染,使其具有抑菌性。作为增效剂,有机酸、β-胡萝卜紊等能够增强茶多酚的抗氧化性能;壳聚糖、食盐等能够增强茶多酚的抑菌活性．维生素类既能够增强茶多酚的抗氧化性能又能增强其抑菌作用。     

应用量子化学方法研究生育酚结构与抗氧化活性的关系

采用分子力学和量子化学从头计算方法,研究分析不同分子结构的生育酚和一些酚类化合物所具抗氧化作用的构效关系。生育酚的抗氧化活性与易释放活泼氢有关,活性大小与Ｏ－Ｈ间电子集居数、前线轨道能级及反应终态能量下降值有关,各种生育酚模型分子的羟基Ｏ－Ｈ电子集居数排列顺序α＜γ≤β＜δ,生育酚自由基转变为醌结构,终态能量下降值顺序为α＞γ≥β＞δ,与文献报道抗氧化活性的结论相一致。应用量子化学指数可以帮助分析具有不同结构的酚类化合物的抗氧化活性     

鸢尾苷抗氧化活性的研究北大核心CSCD

在成功从中草药射干中提取纯化得到鸢尾苷的基础上,应用灵敏、简单易行有效的方法考察鸢尾苷的抗氧化能力。选择氧自由基清除、羟基自由基清除、二苯代苦味肼基自由基清除、烷基自由基清除和抗油脂氧化作用等实验体系进行抗氧化活性的试验。结果显示纯化得到的鸢尾苷的抗氧化作用比维生素C稍强,但比2,6-二叔丁基对甲酚稍弱,表明其具有较显著的抗氧化作用。     

鸢尾苷抗氧化活性的研究

在成功从中草药射干中提取纯化得到鸢尾苷的基础上,应用灵敏、简单易行有效的方法考察鸢尾苷的抗氧化能力。选择氧自由基清除、羟基自由基清除、二苯代苦味肼基自由基清除、烷基自由基清除和抗油脂氧化作用等实验体系进行抗氧化活性的试验。结果显示纯化得到的鸢尾苷的抗氧化作用比维生素C稍强,但比2,6-二叔丁基对甲酚稍弱,表明其具有较显著的抗氧化作用。     

天然抗氧化剂茶多酚的健康作用及其机理

喝茶有助于健康,可以预防一些疾病,这已被流行病学研究所证实。研究表明,茶叶中对身体健康非常有益的物质是具有很强抗氧化能力的茶多酚,茶多酚占茶叶干重的30%左右。茶多酚可以有效地清除氧自由基和脂类自由基,预防脂质过氧化,而且具有抑制肿瘤发生、延缓衰老等功能。本文就茶多酚的健康作用及其分子机理做一综述,其中大部分为我们实验室研究和发表在国内外杂志上的成果。     

茶叶品种及采摘时节对其活性成分的影响分析

本文利用福林酚法、DPPH和ABTS方法比较分析了宣城市特产茶叶涌溪火青、塔泉云雾、敬亭绿雪、溪口云尖的多酚含量及抗氧化活性。同时还对比分析了敬亭绿雪叶片在不同采收时期的多酚含量及抗氧化活性,并利用HPLC-MS分析了制茶过程对叶片多酚成分的影响。研究结果表明:涌溪火青中多酚含量最高为161mg儿茶素/g样品干重,溪口云尖则含量最少为127 mg儿茶素/g样品干重。相对应的,利用DPPH和ABTS法测得涌溪火青的抗氧化活性最高;通过对敬亭绿雪不同采摘时期中茶多酚含量的研究表明,随着采摘时间的延后,其叶片中茶多酚和抗氧化活性均会有所增加。且敬亭绿雪鲜叶片经制茶过程后其茶多酚含量整体上升,咖啡因含量则有所下降。     

黄芩甙、茜草素、茶多酚和Trolox抗氧化能力的增强化学发光研究

应用辣根过氧化物－鲁米诺－过硼酸钠－对碘酚增强化学发光体系测量了四种抗氧化剂清除苯氧自由基的能力,并与其清除超氧阴离子和抗鼠肝微粒体脂质过氧化的能力相比较,结果表明,这四种抗氧化剂在不同系统中都有明显的抗氧化能力,抗氧化剂清除苯氧自由基比清除超氧阴离子的能力更接近于抗鼠肝微粒体脂质过氧化的能力,从而提示增强化学发光法在测定抗氧化剂的抗氧化能力上有良好的应用前景。     

白芽奇兰茶多酚的提取工艺及其抗氧化活性

通过醇提法探究白芽奇兰茶多酚提取工艺及其体外抗氧化活性的作用。通过正交试验优化考察乙醇浓度、液料比、浸提时间和浸提温度对白芽奇兰茶多酚提取率的影响;测定白芽奇兰茶多酚清除·OH、·O_2~-、·DPPH的能力,同时测定了对L929细胞生长的影响及抗H_2O_2氧化作用的能力。结果表明:乙醇体积分数70%、液料比40m L/g、浸提时间165 min、浸提温度75℃,在该条件下,茶多酚提取率最大达81.33 mg/g;白芽奇兰茶多酚具有较强的抗氧化活性,30μg/m L时不影响细胞的正常生长,且可以预防H_2O_2对细胞的损伤。     

一株红茄苳内生烟曲霉菌的分离鉴定及其发酵产物抗氧化活性

【目的】红树林内生真菌生长于特殊的生境,有些菌株能分泌出结构新颖和具有生物活性的物质。从红树林植物红茄苳(Rhizophora mucronata)中分离获得一株内生真菌HQD24,对其进行生物学鉴定和抗氧化活性评价。【方法】综合运用形态结构及ITS r DNA序列分析,HQD24被鉴定为曲霉属(Aspergillus)的烟曲霉(Aspergillus fumigatus)。采用抗氧化多活性模型,2-2′二苯基-1-三硝基苯肼(DPPH)自由基测定法、2′-联氨-双-3-乙基苯并噻唑啉-6-磺酸(ABTS)自由基测定法、超氧自由基测定法、还原Fe~(3+)能力、螯合Fe~(2+)能力对HQD24麦麸发酵提取物的石油醚萃取物、二氯甲烷萃取物、乙酸乙酯萃取物和正丁醇萃取物进行抗氧化活性评价。【结果】经抗氧化活性实验发现不同有机溶剂萃取成分都具有清除DPPH自由基、ABTS自由基、超氧自由基和还原Fe~(3+)、螯合Fe~(2+)的能力,尤其是清除ABTS自由基和超氧自由基,抗氧化活性的能力都随着浓度的增高而增强。当不同有机溶剂萃取粗提物浓度为1.5 g/L时,二氯甲烷萃取物清除ABTS自由基率为71.92%,正丁醇萃取物清除超氧自由基率为62.36%,综合评价,HQD24的发酵产物中具有抗氧化活性的物质主要分布于二氯甲烷萃取粗提物和正丁醇萃取粗提物,其次分布于乙酸乙酯萃取粗提物,石油醚萃取粗提物中抗氧化活性物质含量最少。【结论】研究结果预示红树林内生烟曲霉菌是产生抗氧化活性物质的重要资源,HQD24菌株可以作为进一步实验研究的对象。     

灯盏花乙素及其苷元结构与抗氧化活性关系研究

采用密度泛函理论B3LYP方法对灯盏花乙素及其苷元分子进行几何结构全优化,获得两个化合物的最低能量结构。从分子的几何结构、NBO电荷、酚羟基解离能BDE、绝热电离势IP和前线分子轨道等方面分析了两个化合物的结构与抗氧化活性之间的关系。计算结果表明,C6位的酚羟基为灯盏花乙素及其苷元的最大反应活性位点,灯盏花乙素的抗氧化活性弱于其苷元的抗氧化活性,计算结果与实验结果吻合。天然的糖苷类物质水解为苷元后,其抗氧化活性增强。此外,还考虑了溶剂效应,考察溶剂极性对抗氧化活性的影响。在所有环境中,抽氢反应机制是化合物自由基清除反应的最主要机制。     

Green tea polyphenols inhibit cognitive impairment induced by chronic cerebral hypoperfusion via modulating oxidative stress

Responses to oxidative stress contribute to damage caused by chronic cerebral hypoperfusion, which is characteristic of certain neurodegenerative diseases. We used a rat model of chronic cerebral hypoperfusion to determine whether green tea polyphenols, which are potent antioxidants and free radical scavengers, can reduce vascular cognitive impairment and to investigate their underlying mechanisms of action. Different doses of green tea polyphenols were administered orally to model rats from 4 to 8 weeks after experimentally induced cerebral hypoperfusion, and spatial learning and memory were assessed using the Morris water maze. Following behavioral testing, oxygen free radical levels and antioxidative capability in the cortex and hippocampus were measured biochemically. The levels of lipid peroxidation and oxidative DNA damage were assessed by immunohistochemical staining for 4-hydroxynonenal and 8-hydroxy-2′-deoxyguanosine, respectively. Rats that received green tea polyphenols 400 mg/kg per day had better spatial learning and memory than saline-treated rats. Green tea polyphenols 400 mg/kg per day were found to scavenge oxygen free radicals, enhance antioxidant potential, decrease lipid peroxide production and reduce oxidative DNA damage. However, green tea polyphenols 100 mg/kg per day had no significant effects, particularly in the cortex. This study suggests that green tea polyphenols 400 mg/kg per day improve spatial cognitive abilities following chronic cerebral hypoperfusion and that these effects may be related to the antioxidant effects of these compounds.     

Antioxidative effects of green tea polyphenols on free radical initiated and photosensitized peroxidation of human low density lipoprotein

Antioxidative effects of the main polyphenolic components extracted from green tea leaves, i.e. (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin gallate (EGCG) and gallic acid (GA), against free radical initiated peroxidation of human low density lipoprotein (LDL) were studied. The peroxidation was initiated either thermally by a water-soluble initiator 2,2'-azobis(2-amidinopropane hydrochloride) (AAPH), or photochemically by a triplet sensitizer benzophenone (BP). The reaction kinetics was monitored by the uptake of oxygen and the depletion of alpha-tocopherol (TOH) presented in the native LDL. Kinetic analysis of the antioxidation process demonstrates that these green tea polyphenols are effective antioxidants against both AAPH-initiated and BP-photosensitized LDL peroxidation. The antioxidative action of the green tea polyphenols includes trapping the initiating and/or propagating peroxyl radicals with the activity sequence EC>EGCG>ECG>EGC>GA for the AAPH initiated peroxidation, and reducing the alpha-tocopheroxyl radical to regenerate alpha-tocopherol with the activity sequence of ECG>EC>EGCG>EGC>GA and ECG>EGCG>GA>EC>EGC for the AAPH-initiated and BP-photosensitized peroxidations respectively.     

Evidence for alpha-tocopherol regeneration reaction of green tea polyphenols in SDS micelles

The synergistic antioxidant mechanism of alpha-tocopherol (vitamin E) with green tea polyphenols, i.e., (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin gallate (EGCG), and gallic acid (GA), was studied by assaying the kinetics of the reaction of alpha-tocopheroxyl radical with green tea polyphenols by stopped-flow electron paramagnetic resonance, the inhibition of linoleic acid peroxidation by these antioxidants, and the decay of alpha-tocopherol during the peroxidation. It was found that the green tea polyphenols could reduce alpha-tocopheroxyl radical to regenerate alpha-tocopherol with rate constants of 0.45, 1.11, 1.31, 1.91, and 0.43 x 10(2) M(-1) s(-1) for EC, EGC, ECG, EGCG, and GA, respectively, in sodium dodecyl sulfate micelles. In addition, these second-order rate constants exhibited a good linear correlation with their oxidation potentials, suggesting that electron transfer might play a role in the reaction.     

Antimutagenic activity of green tea polyphenols

For centuries green tea has been a widely consumed beverage throughout the world. It is known to contain a number of pharmacologically active compounds. In this study water extracts of green tea (WEGT) and their major constituents, green tea polyphenols (GTP), were examined for antimutagenic activity. WEGT and GTP were found to significantly inhibit the reverse mutation induced by benzo[alpha]pyrene (BP), aflatoxin B1 (AFB1), 2-aminofluorene, and methanol extracts of coal tar pitch in Salmonella typhimurium TA100 and/or TA98 in the presence of a rat-liver microsomal activation system. GTP also inhibited gene forward mutation in V79 cells treated with AFB1 and BP, and also decreased the frequency of sister-chromatid exchanges and chromosomal aberrations in V79 cells treated with AFB1. The addition of GTP during and after nitrosation of methylurea resulted in a dose-dependent inhibition of mutagenicity. Studies to define the mechanism of the antimutagenic activity of GTP suggest that it may affect carcinogen metabolism, DNA adduct formation, the interaction of ultimate carcinogen or the scavenging of free radicals.     

Cancer chemoprevention by tea polyphenols

Tea is one of the most widely consumed beverages, second only to water. Many experimental researches in laboratory animals demonstrated that tea components had an inhibitory effect on carcinogenesis at a number of organ sites. The inhibitory effects of tea against carcinogenesis have been attributed to the biologic activities of the polyphenol fraction in tea. This review summarizes experimental data on chemopreventive effects of tea polyphenols in various tumor bioassay systems. Many laboratory studies have demonstrated the inhibitory effects of green tea polyphenols, especially (-)-epigallocatechin-3-gallate (EGCG), on carcinogenesis in animals models. The majority of these studies have been conducted in mouse skin tumor models, where tea polyphenols were used either as oral feeding in drinking water or in direct local application. Most studies used 12-O-tetradecanoylphorbol-13-acetate (TPA) or ultraviolet (UV) radiation as the tumor promoter and found anticarcinogenic effects caused by green tea polyphenols. Black tea was also found to be effective, although the activity was weaker than that of green tea in some experiments. Other studies showed that black tea polyphenols-theaflavins exhibited stronger anticarcinogenic activity than did EGCG. Caffeine in tea was also important for tea to prevent tumorigenesis. The molecular mechanisms of the cancer chemopreventive effects of tea polyphenols are not completely understood. They are most likely related to the mechanisms of biochemical actions of tea polyphenols, which include antioxidative activities, modulation of xenobiotic metabolite enzymes and inhibition of tumor promotion. In addition, we have also proposed that tea polyphenols function as cancer chemopreventive agents through modulation of mitotic signal transduction. However, the molecular mechanisms involved in this modulation need further investigation.     

Matrix metalloproteinase inhibition by green tea catechins

We have investigated the effects of different biologically active components from natural products, including green tea polyphenols (GTP), resveratrol, genistein and organosulfur compounds from garlic, on matrix metalloproteinase (MMP)-2, MMP-9 and MMP-12 activities. GTP caused the strongest inhibition of the three enzymes, as measured by fluorescence assays using gelatin or elastin as substrates. The inhibition of MMP-2 and MMP-9 caused by GTP was confirmed by gelatin zymography and was observed for MMPs associated with both various rat tissues and human brain tumors (glioblastoma and pituitary tumors). The activities of MMPs were also measured in the presence of various catechins isolated from green tea including (-)-epigallocatechin gallate (EGCG), (-)-epicatechin gallate(ECG), (-)-epigallocatechin (EGC), (-)-epicatechin (EC) and (+)-catechin (C). The most potent inhibitors of these activities, as measured by fluorescence and by gelatin or casein zymography, were EGCG and ECG. GTP and the different catechins had no effect on pancreatic elastase, suggesting that the effects of these molecules on MMP activities are specific. Furthermore, in vitro activation of proMMP-2 secreted from the glioblastomas cell line U-87 by the lectin concanavalin A was completely inhibited by GTP and specifically by EGCG. These results indicate that catechins from green tea inhibit MMP activities and proMMP-2 activation.     

鸭舌草中抗氧化活性物质的分离与鉴定

采用溶剂萃取法将鸭舌草75%乙醇提取物浸膏分成4个不同组分,并用碘量法测定其抗氧化活性.结果表明,高极性组分正丁醇相具有最强的抗氧化活性,与天然抗氧化剂茶多酚和化学合成抗氧化剂BHT的抗氧化活性相当,显著高于对照.利用柱层析技术对具有高抗氧化活性组分正丁醇相进一步分离纯化,并确定为豆甾醇葡萄糖甙.以BHT为对照对羟自由基进行清除试验,结果表明,与对照抗氧化剂BHT相比,它们对羟自由基具有更高的清除率.     

Targeting oxidative stress response by green tea polyphenols: clinical implications

Abstract

Green tea polyphenols, the most interesting constituent of green tea leaves, have been shown to have both pro-oxidant and antioxidant properties. Both pro-oxidant and antioxidant properties are expected to contribute to modulation of oxidative stress response under ideal optimal dosage regimens. Exposure to a low concentration of a pro-oxidant prior to exposure to oxidative stress induces the expression of genes that code for proteins that induce adaptation in a subsequent oxidative stress. On the other hand, exposure to an antioxidant concurrently with exposure to the oxidative stress affords protection through free radical scavenging or through other indirect antioxidant mechanisms. In any case, the optimal conditions that afford protection from oxidative stress should be defined for any substance with redox properties. Green tea polyphenols, being naturally occurring substances, seem to be an ideal option for the modulation of oxidative stress response. This paper reviews available data on the pro-oxidant and antioxidant properties of green tea polyphenols focusing on their potential on the modulation of oxidative stress response.     

Bioactive components from the tea polyphenols influence on endogenous antioxidant defense system and modulate inflammatory cytokines after total-body irradiation in mice

The present study aimed to evaluate the radioprotective efficacy of green tea polyphenols and the component ingredients against irradiated-induced damage in mice and elucidate the underlying mechanisms. Green tea polyphenols (GTP 50, 50 and 100 mg/kg, p.o. daily) and its four individual components (25 and 50 mg/kg, p.o. daily) were administrated to the irradiated-injured mice for 21 days. The radioprotective effect on the hematopoietic system, serum cytokines, and endogenous antioxidant enzymes was studied. GTP 50 significant revert the irradiated-induced decline in hematological parameters (RBCs, WBCs, Hb), meanwhile, protected antioxidant defense system, as evidenced by decreased of serum lipid peroxidation (malonyldialdehyde) and elevation the antioxidant enzyme superoxide dismutase (SOD). Among the GTP components, catechin showed the best effect on elevation of hematological parameters, and epigallocatechin gallate showed the best antioxidant activity. Moreover GTP and its bioactive components (catechin, epigallocatechin and epigallocatechin-3-gallate) assisted in decreasing the leukocytopenia seen after whole mice irradiation and significantly reduced the elevated serum inflammatory cytokines (TNF-α, IL-1β, and IL-6). Green tea polyphenols have a potential to be developed as radioprotective agents against irradiated-induced toxicity. Furthermore the antioxidant and anti-inflammatory activities of GTP can be attributed to the interaction of the different components through multiple and synergistic mechanisms.     

Green tea polyphenols enhance sodium nitroprusside-induced neurotoxicity in human neuroblastoma SH-SY5Y cells

Oxidative stress is a main mediator in nitric oxide (NO) -induced neurotoxicity and has been implicated in the pathogenesis of many neurodegenerative disorders. Green tea polyphenols are usually expected as potent chemo-preventive agents due to their ability of scavenging free radicals and chelating metal ions. However, not all the actions of green tea polyphenols are necessarily beneficial. In the present study, we demonstrated that higher-concentration green tea ployphenols significantly enhanced the neurotoxicity by treatment of sodium nitroprusside (SNP), a nitric oxide donor. SNP induced apoptosis in human neuroblastoma SH-SY5Y cells in a concentration and time-dependent manner, as estimated by cell viability assessment, FACScan analysis and DNA fragmentation assay, whereas treatment with green tea polyphenols alone had no effect on cell viability. Pre-treatment with lower-dose green tea polyphenols (50 and 100 microm) had only a slightly deleterious effect in the presence of SNP, while higher-dose green tea polyphenols (200 and 500 microm) synergistically damaged the cells severely. Further research showed that co-incubation of green tea polyphenols and SNP caused loss of mitochondrial membrane potential, depletion of intracellular GSH and accumulation of reactive oxygen species, and exacerbated NO-induced neuronal apoptosis via a Bcl-2 sensitive pathway.