EGCG3 Me提取与分离工艺研究

采用HPLC、聚酰胺树脂、HPTLC等技术手段,进行EGCG3Me的提取与分离纯化研究.通过正交实验表明,EGCG3Me最优提取工艺条件为:乙醇体积分数70%、回流时间3 0 min、回流温度80℃、料液比1:10,质量分数为0.89%.采用40%酒精、60%酒精进行冼脱时,有大量EGCG3Me富集.以甲醇:氯仿...     

茶黄素与EGCG抑制体内外β-淀粉样蛋白1-42水平及其诱导的神经细胞氧化损伤

通过模拟生理条件体外实验,将β-淀粉样蛋白1-42(Aβ42)与EGCG和4种茶黄素单体分别按照1︰1和1︰5比例进行孵育,采用硫黄素T荧光检测β-折叠结构的生成量,结果表明,EGCG与茶黄素均能明显降低β-折叠结构生成,从而抑制Aβ42聚集;此外,通过建立20μmol·L~(-1) Aβ42诱导人神经母细胞瘤SH-SY5Y细胞损伤模型,将不同浓度的EGCG或茶黄素(10、50、100μmol·L~(-1))处理后,MTT法检测细胞存活率,同时,检测细胞内活性氧(ROS)、谷胱甘肽过氧化物酶(GSH-Px)及丙二醛(MDA)等抗氧化指标,结果表明,EGCG与茶黄素可抑制因Aβ42诱导SH-SY5Y细胞活力下降及氧化损伤。体内实验中,通过10mg·kg~(-1)·d~(-1)的EGCG或茶黄素处理快速老化模型小鼠(SAMP8),10周后检测小鼠血清Aβ42及晚期糖基化终末产物(AGEs)含量,结果表明,EGCG和茶黄素可显著降低SAMP8小鼠血清中Aβ42及AGEs含量。本研究表明了茶黄素和EGCG可抑制Aβ42聚集纤维化及Aβ42导致的神经氧化损伤,从而对阿尔茨海默病具有一定保护作用。     

茶树EGCG合成过程相关的Ankyrin基因的克隆与表达分析

运用RACE技术,从茶树新品系1005嫩芽中克隆出Ankyrin基因全长c DNA(2 034 bp),5′UTR和3′UTR分别为353 bp和55 bp,编码541个氨基酸,命名为CS-Ankyrin。基因全长序列在线blast比对分析结果表明,该基因与葡萄、蓖麻、可可和杨树的Ankyrin序列的一致性分别为78%、78%、77%和77%。生物信息学分析显示,CS-Ankyrin锚蛋白重复序列是由5个ANK单元组成,该蛋白是定位在质膜上起作用的跨膜疏水蛋白,但疏水性较差;系统进化树分析表明,该基因编码的氨基酸与芝麻的亲缘关系最为接近。比较CS-Ankyrin在不同发育阶段叶片的表达和EGCG含量变化结果表明,CS-Ankyrin基因在3个品系不同样品的表达趋势与其EGCG含量变化趋势一致,芽头二叶四叶;亚细胞定位试验结果表明,CS-Ankyrin蛋白定位在细胞膜上起作用。推测该蛋白可能参与EGCG的储存和跨膜运输。     

EGCG与锌离子互作对PC-3细胞能量代谢的影响

采用Hoechst33258荧光染色法观察EGCG、Zn2+和EGCG+Zn2+对前列腺癌PC-3细胞凋亡的诱导作用;采用HPLC法检测了EGCG、Zn2+和EGCG+Zn2+对PC-3细胞内腺苷酸(ATP、ADP、AMP)含量的影响,并分析了能量负荷(EC)和ATP/ADP比值。结果表明,Hoechst33258染色后正常细胞发出均匀微弱的蓝色荧光,细胞核未见异常,EGCG、Zn2+和EGCG+Zn2+处理后凋亡的PC-3细胞都发出较强的蓝色荧光,细胞核DNA断裂及染色体高度浓缩;EGCG、Zn2+及二者混合物处理后细胞内总腺苷酸含量、EC及ATP/ADP比值都下降,表明EGCG与Zn2+对PC-3细胞能量代谢都存在明显的抑制作用。     

七种甲酯化植物油及其复配助剂对噁唑酰草胺的增效作用

为了筛选出高效的除草剂桶混助剂,显著增加噁唑酰草胺药效,减少有效成分用量,以玉米油、花生油、菜籽油、大豆油、葵花籽油、蓖麻油和芝麻油7种植物油为原材料,采用碱催化酯交换原理合成了7种甲酯化植物油,将其按不同比例复配并添加乳化剂后得到了20种桶混助剂;通过温室盆栽法测定了20种助剂对噁唑酰草胺的增效作用。结果表明:当甲酯化植物油助剂的体积分数为喷液量的0.5%时,能显著提高噁唑酰草胺药液在稻稗叶面上的沉积量,沉积量增加范围为11.17%~143.60%;有效降低噁唑酰草胺药液的表面张力和接触角,降低范围分别为9.67%~27.34%和8.72%~65.60%。20种甲酯化植物油助剂对噁唑酰草胺防除稻稗均有一定的增效作用,其中增效作用最显著的为甲酯化植物油助剂JZ-4(配方为:m(甲酯化花生油):m(甲酯化玉米油)=2:1,乳化剂m(OP-7):m(PEG-400):m(ZR-5)=1:1:0.5,含量为甲酯化植物油质量的20%);与未添加助剂的噁唑酰草胺有效剂量120 g/hm^2相比,添加甲酯化植物油助剂JZ-4后,株死亡率提高45.00%,鲜重抑制率提高了25.53%。最后,通过综合分析筛选出对噁唑酰草胺防除稻稗增效作用最好的助剂为甲酯化植物油助剂JZ-4。     

茶叶中EGCG功效研究进展

表没食子儿茶素没食子酸酯(EGCG)药理作用已经得到了国内外一些研究人员的认可。近年来科学工作者已经越来越多将注意力集中于儿茶素上,尤其是其中的单体之一表没食子儿茶素没食子酸脂(EGCG)最引人注目。本文就近年来对EGCG药理作用、机理进行阐述,为探索EGCG的药用价值提供参考依据。     

绿茶及茶多酚药理作用研究进展

茶消费量占全球饮料消费量第2位,普及性仅次于水.绿茶的化学成分主要包括多酚、咖啡因和氨基酸,绿茶中含有丰富的儿荼素,其中茶多酚是最丰富的.绿茶及其中的多酚在治疗多种疾病方面发挥积极作用,如癌症、糖尿病、心血管疾病、肥胖症等.对茶和茶多酚相关的药理特征进行了重点讨论,希望能开拓新的研究领域,并鼓励对公众健康问题进行研究.     

Protective effects of EGCG on Bifenthrin-Induced Oxidative Stress in the Human Embryonic Lung Fibroblast Cell Line HFL-I

Bifenthrin （BF） is an important type I synthetic fluorinated pyrethroid insecticide and acaricide.Previous investigations have indicated that the metabolisms of BF in human cells were through oxidative processes,and cytotoxicity was induced by the oxidative stress.In this study,the protective effects of EGCG,which is a major individual of green tea polyphenols,on the human embryonic lung fibroblast cell line HFL-I exposed to BF were investigated.The results showed that BF could induce oxidative stress leading to cytotoxicity in HFL-I cells.The pretreatment of EGCG at low concentrations significantly recovered the cell viability and morphology,inhibited excess generation of ROS,enhanced antioxidant enzyme activities and avoided loss of mitochondrial membrane potential.The results suggested that EGCG might eliminate the BF-induced damage in HFL-I cells.     

A Novel Liquid Multi-Phytonutrient Supplement Demonstrates DNA-Protective Effects

This study explored the DNA protective (anti-mutagenic) effects of an oral, liquid, multi-phytonutrient dietary supplement containing a proprietary blend of fruits, vegetables and aloe vera concentrated components in addition to a proprietary catechin complex from green tea (VIBE Cardiac & Life, Eniva Nutraceuticals, Anoka, MN; herein described as “VIBE”). This study tested the hypothesis that VIBE would reduce DNA damage in skin cells exposed to UVR. Human epidermal cells, from the cell line A431NS, were treated with 0% (control), 0.125%, 0.5%, 1% and 2% VIBE, and then exposed to 240 J/m² UVR. The amount of DNA damage was assessed using the COMET assay. At each concentration tested, a significantly smaller amount of DNA damage was measured by the COMET assay for the VIBE treated cells compared to the control cells exposed to UVR without VIBE. The dose response curves showed a maximal response at 0.5% VIBE with a threefold reduction in COMET tail density compared to the control samples without VIBE (p < 0.001). Additional research is warranted in human clinical trials to further explore the results of this study which demonstrated the DNA protective and anti-mutagenic effects of VIBE for human skin cells exposed to UVR-induced DNA damage.