花青素论文1稿
原花青素的提取和对美容的作用(论文)
原花青素的提取和对美容的作用【摘要】原花青素(Procyanidins，PC)是从多种植物中提取的一类物质。
具有多种生物活性，是一种很强的抗氧化剂，能清除自由基抑制脂质过氧化发生，PC的低聚体发挥了重要作用。
它对皮肤有很好的保护作用，主要是因为原花青素具有抗氧化、改善皮肤过敏、美容养颜、祛斑的作用。
本作品主要是在已知方法的基础上探求更简便、高效的方法来提取葡萄糖中的原花青素，提高原料利用率，减少资源浪费。
并且研究其对美容的作用。
【关键词】原花青素高效抗氧化保护美容0引言原花青素(Procyanidins,PC)是植物王国中广泛存在的一大类多酚类化合物的总称，起初统归于缩合鞣质或黄烷醇类，随着分离鉴定技术的提高和对此类物质的深入研究与深刻认识，现已成为独树一帜的一大类物质并称之为原花青素。
原花青素主要分布在葡萄、银杏、大黄、山楂、小连翘、花旗松、日本罗汉柏、白桦树、野草莓、海岸松、甘薯等植物中，但研究发现葡萄籽提取物中原花青素的含量最高。
20世纪80年代以来，人们对数十种植物的原花青素低聚体和高聚体进行了生物、药理活性的研究，发现原花青素是一种很强的抗氧化剂，其具有的特殊抗氧活性和清除自由基的能力为其在化妆品领域中的应用开辟了广阔前景，在化妆品领域有很大的发展空间和前景。
1原花青素的结构原花青素(Proanthocyanidins,简称PC)是植物王国中广泛存在的一大类多酚化合物的总称。
原花青素在自然界中广泛存在，人们对它的研究已有30多年的历史，几十年来，在涉及的众多植物中，葡萄中的花青素具有含量高、原料成本低的优势。
1961年，德国Kralf 的等人从山楂新鲜果实的乙醇提取物中首次分解出两种多酚化合物，1967年，美国Jsolyn M.A等人又从葡萄皮和葡萄籽提取物中分离出4中多酚化合物，他们得到的多酚化合物在酸性介质中加热均可产生花青素。
早在50年代，法国科学家就发现可以在松树皮中提取大量的原花青素，其提取物中可含85%的原花青素。
花青素研究报告
花青素研究报告
花青素是一种独特的自然黄酮，在植物类黄酮中占有重要地位。
位于己醛和精氨酸家族黄酮化合物之间，它有两个共价双键和一个负
电的芳香环。
被认为可以被动物和植物体内有效吸收，并且可以直接
以原形参与生物过程。
花青素作为一种天然有机化合物，具有多种生物活性，主要表现
在抗氧化性、抗疲劳性、抗菌抗炎、抗黄褐斑、抗肿瘤。
它能够帮助
改善免疫力，还有降低胆固醇和血脂，对于抗衰老、肝保护、改善贫
血也有显著的效果。
研究表明，花青素可促进皮肤协调改善皮肤龟裂、血管松弛痉挛，降低皮肤的老化，提高皮肤的纹理，使皮肤紧致有光泽。
再者，花青素作为一种抗氧化剂，可减少机体，特别是对老年人
来说，可以延缓衰老，抢救体内自由基对人体造成的危害，增强机体
的免疫力。
它同时具有抗衰老、抗癌、抗炎、抗氧、抗菌等作用。
因此，花青素具有多项药理作用，可以作为最有效的保健品之一。
在保健品和其他产品的开发过程中，可以将其用作有效成分。
从日常
生活中一些常见的食物如蔬菜、水果、豆类、坚果等中，也可以摄取
花青素。
浅谈花青素的生理作用及发展机制
浅谈花青素的生理作用及发展机制浅谈花青素的生理作用及发展机制［摘要］：花青素是一种广泛存在于植物中水溶性的色素，属于类黄酮，性质比较稳定。
因其安全、无毒、资源丰富，已被用作为一种天然食用色素即食品添加剂，在食品、化妆、医药等方面有着巨大的应用潜力。
因此，开发和应用天然色素已成为世界食用色素发展的总趋势。
花青素具有很强的清除自由基的能力，并且具有抗氧化、抗炎、抗过敏、抗癌、护肝、预防心脑血管疾病、提高记忆力、保护视力、改善睡眠、抗辐射等作用。
为此本文对花青素的生理作用及发展机制作一综述，以提高我国对花青素这一类类黄酮植物化学物的进一步研究。
［关键字］：花青素，生理作用，发展机制。
花青素是一种广泛存在于植物中水溶性的色素，属于类黄酮类植物化学物，是植物和果实中的一种主要呈色物质。
目前发现花青素类色素广泛存在于紫甘薯、葡萄、血橙、蓝莓、红莓、樱桃、茄子皮、桑葚、山楂皮、紫苏、牵牛花等植物中。
现代医学证明花青素对人类具有多种医疗保健作用，如抗氧化、抗炎、抗过敏、抗癌、护肝、预防心脑血管疾病、提高记忆力、保护视力、改善睡眠、抗辐射等作用。
其抗癌、保护心脑血管、美容等功效越来越显著，更是受到人们的青睐。
1、抗氧化作用不断的科学研究证实，自由基与癌症、心脏病等一些慢性疾病的发生有着密切的关系，清除自由基和抗氧化是营养保健的重要前提和基础。
自由基的衰老学说认为，细胞衰老、器官退化都与体内自由基过多有关。
法国科学家马斯魁勒博士发现花青素是天然存在的强效自由基清除剂，是目前科学界发现的防治疾病、维护人类健康最直接、最有效、最安全的自由基清除剂，最受专家重视的一种抗氧化剂，郑建仙提出OPC’s是消除自由基的最强抗氧化剂，而花青素抗氧化性是传统的抗氧化剂Vc的20倍，VE的50倍，是一种很好的氧自由基清除剂和脂质过氧化抑制剂。
Castillo等研究表明：在清除自由基、抗氧化能力上，花青素＞芦丁＞儿茶素＞洋芫荽苷＞抗坏血酸。
花青素新论文张志新
茄子中花青素的提取张志新（北京电子科技职业学院，10生物技术20100005032）摘要：本文通过对不同茄子的皮和瓤进行破碎和吸光度值的测定，提取和测定不同品种茄子中花青素的含量。
结果表明：圆茄子中花青素含量最高，圆茄中比长茄中的花青素含量高约6.4%，但提取率却比长茄子低0.7%.花青素溶液应在避光、低温且弱酸弱碱的条件下保存。
茄子皮中花青素的含量相对于茄子瓤中花青素含量高。
因此，从茄子皮中提取天然花青素具有广阔的前景。
关键词：茄子花青素含量前言：随着生活水平的提高，人们对食品安全的关注日益提高。
虽然合成色素色泽鲜艳、稳定性好、价格低廉，但因其合成毒性问题，使得天然花青素在食品、医药和化妆品等行业上逐渐得到重视。
天然花青素类毒性低，同时具有保健功能和鲜明的色调，安全性得到了人们的一致认可。
在我国现阶段，天然花青素尤其是紫红色花青素多以新鲜的果蔬为原料，我们选取紫长茄子和圆茄子对其中进行提取。
茄子学名为Solanum melongena L.，别名落苏、酪酥、昆仑瓜等，为茄科茄属以浆果为产品的一年生草本植物。
茄子味道鲜美，营养丰富，不仅是我国广大城乡人民喜爱的主要蔬菜之一，而且是一味中药［1］，茄子皮中富含VE和VP，这是其他蔬菜所没有的，因此从茄子中提取花青素具有一定的开发价值。
目前，关于茄子中花青素的研究集中于单一品种茄子花青素的提取工艺、稳定性和抗氧化性方面，如王川[2]得出茄子紫色素的最佳提取剂为无水乙醇、提取温度40℃，而针对不同品种之间进行比较研究，还尚未见报道。
本实验以不同果型的茄子品种为试材，探讨不同品种茄子果实花青素含量，进而筛选出花青素含量高且稳定性好的茄子品种，为今后保健食品的开发提供方向性的提示参考。
1·材料与方法1.1材料与试剂供试的茄子长茄为布朗、黑又亮，圆茄为天津快圆茄；均达到了成熟度，洗净备用。
1.2实验器材菜刀、榨汁机、烧杯、玻璃棒、量筒、电子天平、恒温水浴锅、离心管、离心机、石英比色皿、紫外分光光度计。
关于花青素实验的作文
关于花青素实验的作文在神奇的化学世界里，有一个让我痴迷不已的实验——花青素实验。
这个实验就像是一场色彩的魔法秀，充满了惊喜和趣味。
那是一个阳光明媚的周末，我心血来潮，决定在家自己动手尝试这个听起来就很酷炫的花青素实验。
我把自己关在小小的实验室里（其实就是家里的书房），满心期待地开始了这场奇妙之旅。
实验前的准备工作可不少。
我翻箱倒柜找出了所需的材料：紫甘蓝、白醋、小苏打、几个透明杯子还有搅拌棒。
紫甘蓝被我从冰箱里拎出来的时候，它看起来就像一个穿着紫色晚礼服的胖娃娃，圆滚滚、水灵灵的。
我小心翼翼地把紫甘蓝切成小块，然后放入锅中煮。
随着水温的升高，紫甘蓝在锅里翻腾着，就像一群紫色的小精灵在欢快地跳舞。
煮了一会儿，水开始变色了，从无色渐渐变成了淡紫色。
这时候，我把煮好的紫甘蓝水过滤到一个大碗里，那深紫色的液体，神秘而诱人，仿佛藏着无尽的秘密。
接下来就是最激动人心的时刻啦！我把紫甘蓝水分别倒进几个透明杯子里，大概每个杯子都装了半杯左右。
首先，我往第一个杯子里倒入了一些白醋。
就在白醋接触到紫甘蓝水的瞬间，奇妙的事情发生了！杯子里的液体迅速变成了粉红色，就像是羞涩少女的脸蛋。
我瞪大眼睛，忍不住“哇”了一声，心里满是惊喜。
然后，我又往第二个杯子里加入了小苏打。
这一次，液体变成了蓝色，那种蓝就像是晴朗天空的颜色，清澈而明亮。
我拿着搅拌棒轻轻搅拌着，看着颜色均匀地变化，感觉自己就像是一个神奇的魔法师。
第三个杯子里，我尝试着同时加入白醋和小苏打。
液体在杯子里翻滚着，颜色一会儿变成粉色，一会儿又变成蓝色，就像是一场色彩的大战，你来我往，好不热闹。
为了更清楚地观察变化，我把杯子一字排开放在桌子上，眼睛一眨不眨地盯着。
阳光透过窗户洒在杯子上，折射出五彩斑斓的光芒，美极了！在这个实验过程中，我也遇到了一些小插曲。
有一次，我不小心把紫甘蓝水洒在了桌子上，赶紧手忙脚乱地拿纸巾擦拭，结果弄得桌子上一片狼藉。
还有一次，因为倒白醋的时候太着急，一下子倒多了，颜色变得特别深，都快成紫红色了，让我有点小失落。
花青素的研究进展及其应用
花青素的研究进展及其应用一、本文概述花青素是一类广泛存在于自然界中的天然色素，因其独特的色彩和生物活性，在食品、医药、化妆品等多个领域具有广泛的应用前景。
近年来，随着科学技术的不断发展，花青素的研究逐渐深入，其在抗氧化、抗炎、抗肿瘤等方面的生物活性得到了广泛关注。
本文旨在综述花青素的研究进展，包括其提取工艺、生物活性、作用机制等方面的最新研究成果，同时探讨花青素在各个领域的应用现状及其未来发展趋势。
通过本文的阐述，旨在为花青素的研究与应用提供全面的参考，为相关领域的研究者和从业人员提供有价值的指导和帮助。
二、花青素的结构与性质花青素是一类广泛存在于自然界中的天然色素，其化学结构属于黄酮类化合物，主要存在于植物的花、果实、茎和叶等部位。
花青素的基本结构是由两个苯环通过一个吡喃环连接而成，呈现出独特的蓝色或紫色。
这些色彩不仅使植物呈现出五彩斑斓的外观，而且赋予了植物诸多生物活性。
花青素的主要性质包括其稳定性、水溶性以及抗氧化性等。
花青素在水溶液中呈现鲜艳的色泽，且其颜色随pH值的变化而变化，这一特性使其在食品工业中具有广泛的应用前景。
花青素具有较强的抗氧化性，能够有效清除体内的自由基，从而起到延缓衰老、预防疾病的作用。
在结构上，花青素具有多种类型，如黄酮醇、黄酮、黄烷酮等，不同类型的花青素在结构和性质上存在一定的差异。
这些差异使得花青素在生物活性方面表现出多样性，如抗炎、抗癌、抗心血管疾病等。
花青素的结构与性质使其成为一类具有重要研究价值的天然色素。
通过深入研究花青素的结构与性质，不仅可以揭示其在植物生长发育和逆境响应中的生物学功能，还可以为花青素在食品、医药等领域的应用提供理论依据和技术支持。
三、花青素的提取与分离花青素作为一类具有丰富生物活性的天然色素，其提取与分离技术在近年来得到了广泛的研究与发展。
花青素的提取主要依赖于其溶于有机溶剂的特性，常用的提取方法包括溶剂提取法、超声波辅助提取法、微波辅助提取法以及超临界流体萃取法等。
花青素的研究进展
花青素的研究进展1、前言。
花青素主要在人类日常生活的利用上有较大的前景。
是自然界一类广泛存在于植物中的水溶性天然色素，可以随着细胞液的酸碱改变颜色，属类黄酮化合物。
花青素为人类发展提供了许多好处。
在维持人体身体健康方面，花青素是一种强有力的抗氧化剂，它能增强人体血管的弹性，改善循环系统和增进皮肤的光滑度，抑制炎症和过敏，改善关节柔韧度等；在人类的生产工业方面，它也大大促进了其发展，如用于制造成化妆品，保健品等。
然而，目前食品工业上所用的色素多为合成色素，几乎都有不同程度的毒性，长期使用会危害人的健康，因此天然色素就越来越引起了科研领域的关注。
由于至今国内市场上还没有花青素纯品，所以提取到高纯度的花青素对花色苷类色素的深入研究与开发提供必备的表征条件和理论依据，并且有助于它的工业利用。
2、主体1)花青素的合成原理以及成因分析。
a、花青素形成的基因表达和调控。
花颜色形成过程的调控是很复杂的，花色素生物合成是由环境刺激因子如光、温度和营养供给调节的；此外还受内部因子的调节，如生长调控子、代谢物以及组织的特殊发育阶段，不同的调控因子控制了生物合成途径的不同部分，不同的调控因子之间也存在着相互作用，正是这些调控因子的协同作用才使世界呈现出各种各样的色彩。
b、影响花色的因素。
GA、光和糖信号相互作用协调控制花色素苷合成和调控参与花瓣细胞扩展的相关途径中特异的转录调节因子，在向花发育的第二阶段转换时，相继活化这些途径，以完成花的发育和着色。
GA信号可能与糖信号相互作用，糖可能促进GA信号转导途径上游组分的活性，而诱导特异转录因子的表达，继而诱导各种GA响应基因。
另外，花色素苷合成之后，本身的羟基化、甲基化、糖基化及酰基化、花色素苷同其它色素的共着色也都影响着花的最终色彩。
另外，对鸡冠花的研究表明，最适合鸡冠花悬浮细胞体系生产花色素苷的培养基是MS+2,4．D21amoFL+KT21~mol／L+蔗糖292mmol／L，光是诱导花色素苷积累的主要因素，最合适光照度为70ttmol／s·m2，继代培养前三代花色素苷积累量逐渐上升，到第四代开始稳定。
花青素提取实验论文[终稿]
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紫甘蓝中花青素的提取研究【摘要】蓝花青素具有很强的抗氧化作用，具有清除体内自由基、过敏、保护胃粘膜等多种功能，引起了国内外学者广泛关注。
目前抗变异、抗肿瘤、抗，对花青素的研究主要集中于花青素的提取、分离纯化、热稳定性、抗氧化性及其生理功能等方面。
本文主要研究了紫甘蓝花青素的提取工艺;用大孔树脂初步纯化紫甘蓝花青素;对紫甘蓝花青素纯度鉴定。
采用“溶剂提取、萃取、树脂纯化、薄层色谱”相结合的方案对紫甘蓝花青素进行了分离纯化。
【关键词】紫甘蓝花青素提取分离纯化1.1引言花青素作为可使用色素之一，具有多种生物学作用，将广泛用于食品加工、医药保健品、化妆品行业。
虽然国内外己开展了一些研究，主要集中在花青素粗品的提取方法的研究方面，而对紫甘蓝花青素的组成及分子结构鉴定、生物学活性、药理作用的研究还很少，还需要大量数据为其进一步开发和利用提供理论依据。
2.1材料与方法2.1.1实验材料新鲜紫甘蓝2.1.2实验方法溶剂提取、萃取、树脂纯化、薄层色谱2.2主要仪器、试剂分析天平、外分光光度计、环水式多用真空泵、心机、旋转蒸发仪、恒温水浴锅、无水乙醇、甲醇、孔树脂、浓盐酸。
2.3实验方法2.3.1紫甘蓝色素的提取取新鲜80G的紫甘蓝叶片于大杯中加入一定的浸提剂，吸取一定体积的浸提液于 1 Oml比色管中，用浸提剂稀释至刻度，用浸提剂做空白，测定其对520nm光的吸光度。
采用溶剂提取法。
称取紫甘蓝80g，用500ml的60%乙醇和1%盐酸混合液进行捣碎浸提8层纱布过滤，4℃条件下静置3h，离心测OD 值。
2.3.2紫甘蓝色素的初步纯化大孔树脂预处理的方法:将待处理的大孔树脂装入柱中，用95%乙醇浸泡24h一用95%乙醇2}4BV冲洗一用去离子水洗至无醇味一5%氢氧化钠溶液2}4BV冲洗树脂柱一水洗至中性一10%乙酸2}4BV冲洗通过树脂柱一水洗至中性，备用。
滤液用5倍的纯水稀释，大孔吸附树脂法分离，往吸附柱中先用15%乙醇除杂，再用60%乙醇洗脱收集洗脱液；用四分之一的盐酸在90℃条件下水解1h，再加5倍纯水稀释；大孔吸附树脂再次分离，此时用水除杂，无水乙醇洗脱收集；2.3.3花青素的浓缩结晶无水乙醇洗脱液用旋转蒸发仪浓缩，放冰箱中等待是否有结晶甲醇：盐酸=4:1做展开剂测纯度3.1 实验结果及讨论3.1.1浓度计算紫甘蓝捣碎榨汁后得到深紫色溶液，过滤静置稀释40测得OD值为0.865由曲线可得到花青素含量为1.98mg/ml或 6.94mmol/ml3.1.2结果讨论关于天然色素的提取纯化。
《2024年马铃薯花瓣花青素调控基因F的克隆与功能验证》范文
《马铃薯花瓣花青素调控基因F的克隆与功能验证》篇一一、引言随着现代农业的不断发展，对于作物品质的提升及对疾病和环境的抗性增强已成为农业研究的热点。
马铃薯作为全球重要的农作物之一，其品质和抗性也备受关注。
花青素是植物中一种重要的次生代谢产物，具有抗氧化、抗癌等功效，而马铃薯花瓣中的花青素含量直接影响其商品价值和营养价值。
近年来，花青素调控基因的研究成为植物基因工程和育种的重要领域。
本论文以马铃薯花瓣花青素调控基因F为研究对象，对其克隆与功能进行验证，以期为马铃薯品质改良提供理论依据。
二、材料与方法1. 材料本实验以马铃薯为研究对象，选取具有高花青素含量的品种进行实验。
同时，我们获取了与花青素合成相关的已知基因序列，用于后续实验的对比分析。
2. 方法（1）基因克隆通过PCR技术，从马铃薯花瓣中扩增出花青素调控基因F的DNA序列。
对PCR产物进行纯化、测序，获得基因F的完整序列。
（2）生物信息学分析利用生物信息学软件对基因F进行序列分析，包括开放阅读框预测、蛋白质结构预测等。
（3）功能验证构建基因F的过表达和沉默载体，通过遗传转化技术将其导入马铃薯中，观察转基因马铃薯花瓣中花青素含量的变化，从而验证基因F的功能。
三、实验结果1. 基因克隆结果通过PCR技术成功扩增出马铃薯花瓣花青素调控基因F的DNA序列，测序结果与已知序列比对，确认了基因F的完整性。
2. 生物信息学分析结果基因F的序列分析表明，其具有典型的调控基因特征，如包含开放阅读框、具有典型的蛋白结构域等。
进一步预测表明，基因F可能参与花青素的合成和调控。
3. 功能验证结果将基因F的过表达和沉默载体分别导入马铃薯中，观察转基因马铃薯花瓣中花青素含量的变化。
结果显示，过表达基因F的转基因马铃薯花瓣中花青素含量显著提高，而沉默基因F的转基因马铃薯花瓣中花青素含量降低。
这表明基因F在马铃薯花瓣中确实参与了花青素的合成与调控。
四、讨论本实验成功克隆了马铃薯花瓣花青素调控基因F，并通过生物信息学分析和功能验证表明，该基因在花青素合成过程中发挥重要作用。
《基于花青素的智能食品包装薄膜的制备与性能研究》范文
《基于花青素的智能食品包装薄膜的制备与性能研究》篇一一、引言随着科技的发展和人们生活水平的提高，食品包装材料的研究与开发越来越受到关注。
智能食品包装薄膜因其具有保护食品、延长保质期、提供信息等特性，成为当前研究的热点。
本文以天然色素花青素为原料，探讨其制备智能食品包装薄膜的方法，并对其性能进行研究。
二、花青素简介花青素是一种天然色素，具有抗氧化、抗衰老等生物活性。
它广泛存在于植物中，如蓝莓、黑米、紫薯等。
花青素因其独特的化学结构，使其在可见光范围内具有强烈的颜色变化特性，这一特性使其在智能食品包装领域具有广阔的应用前景。
三、制备方法基于花青素的智能食品包装薄膜的制备主要包括以下几个步骤：原料准备、花青素提取、薄膜制备、后处理等。
首先，选取富含花青素的植物原料进行提取，通过合适的提取工艺获得花青素。
然后，将提取的花青素与成膜材料混合，通过一定的工艺手段制备成薄膜。
最后，对薄膜进行后处理，以提高其性能和稳定性。
四、性能研究1. 光学性能：本研究所制备的基于花青素的智能食品包装薄膜具有优良的光学性能，可在不同环境下呈现不同的颜色变化。
这一特性可实现食品新鲜度、保质期等信息的可视化显示。
2. 机械性能：通过对薄膜进行拉伸、撕裂等测试，发现其具有较好的机械性能，可满足食品包装的实际需求。
3. 阻隔性能：本研究所制备的薄膜具有良好的阻隔性能，可有效阻止氧气、水分等对食品的侵害，从而延长食品的保质期。
4. 生物活性：由于花青素的加入，使得薄膜具有一定的生物活性，可抑制细菌、霉菌的生长，有利于食品的保存。
5. 稳定性：通过对薄膜进行加速老化、温度循环等测试，发现其具有良好的稳定性，可在不同环境下保持其性能的稳定。
五、结论本文以花青素为原料，成功制备了基于花青素的智能食品包装薄膜。
该薄膜具有优良的光学性能、机械性能、阻隔性能和生物活性，可有效保护食品，延长保质期，提供信息等功能。
同时，由于花青素的天然来源和独特的化学结构，使得该薄膜具有较高的安全性和环保性。
花青素在农业上的应用
花青素在农业上的应用花青素是一类天然的植物色素，广泛存在于植物中，尤其是在花朵和果实中含量较高。
近年来，随着对花青素研究的深入，人们逐渐发现了花青素在农业上的广泛应用价值。
花青素在农业领域中被广泛应用于植物生长调节和病害防治方面。
研究发现，花青素具有抗氧化和抗病原微生物的能力，能够增强植物的抗病能力，提高植物对环境逆境的适应性。
此外，花青素还能够调节植物的生长发育过程，促进植物的生长和发育，提高植物的产量和品质。
花青素在植物的抗逆性方面也具有重要作用。
在农业生产中，植物常常面临各种环境胁迫，如干旱、高温、寒冷等。
而花青素作为一种天然的抗氧化剂，可以帮助植物抵御氧化应激，减轻环境胁迫对植物的伤害。
此外，花青素还能够通过调节植物的生理代谢过程，提高植物对环境逆境的适应性。
花青素还可用于植物的抗虫害和抗除草剂方面。
研究表明，花青素具有抗虫害的作用，可以抑制害虫的发生和繁殖，减少农药的使用。
同时，花青素还能够通过调节植物的生长发育过程，提高植物对除草剂的抗性，减少对环境的污染。
花青素还可以用于农产品的加工和保鲜方面。
花青素作为一种天然色素，可以用于食品、饮料、化妆品等的加工中，不仅能够增加产品的色彩和口感，还具有一定的保健功能。
同时，花青素还可以用于农产品的保鲜和延长货架期，减少农产品的损耗，提高农产品的附加值。
花青素在农业领域中具有广泛的应用价值。
通过应用花青素，不仅可以提高植物的产量和品质，增加农产品的附加值，还可以减少对环境的污染，促进农业的可持续发展。
因此，进一步研究和应用花青素在农业上的作用，对于提高农业生产效益和保护生态环境具有重要意义。
原花青素及其功能
《食品微生物专题》课程论文课程：食品营养学课程论文论文题目：原花青素及其生理作用姓名学号：白家玮 ******** 指导老师：***年级专业： 2015 食品工程所在学院：生物系统工程与食品科学学院2016年1月12日原花青素及其生理作用摘要：原花青素是一类广泛存在于自然界中的黄烷-3-醇类化合物。
本文综述了近年来国内外关于原花青素的提取、分离纯化、生物活性等方面的研究进展, 为未来的进一步研究提供参考。
关键词：原花青素化学结构分离纯化活性Abstract:The procyanidins is a kind of -3- alcohol compound which is widely existed in thenatural world.This paper reviewed the research progress on extraction, purification and biological activity of the extraction of procyanidins at home and abroad in recent years and provides references for further research in the future.Keywords:procyanidins Chemical structure Separation and purificationactivity原花青素属于缩合单宁，是广泛存在于各种植物的核、皮或种籽等部位[1~5]的一种多酚化合物。
人们对它的研究已有五十余年的历史，特别是八十年代以来，随着技术手段的进步和人们对于健康产业的日益关注，世界上有关原花青素的研究日益广泛和深入。
最早，由于原花青素强大的抗氧化作用，而广泛应用于食品、药品和化妆品等领域。
近年来又发现原花青素具有抗癌活性和保护心血管的功能，而被极大地拓宽了其的营养价值。
花青素论文1稿
2015年度本科生毕业论文（设计）桉树叶中原花青素的提取英文题目Extraction of anthocyanins fromleaves of Eucalyptus院（系）：资源环境学院专业：化学年级： 2012级学生姓名：王兴刊学号： 120640135导师及职称：张星和（助教）2015年 06月毕业论文（设计）原创性声明本人所呈交的毕业论文（设计）是我在导师的指导下进行的研究工作及取得的研究成果。
据我所知，除文中已经注明引用的内容外，本论文（设计）不包含其他个人已经发表或撰写过的研究成果。
对本论文（设计）的研究做出重要贡献的个人和集体，均已在文中作了明确说明并表示谢意。
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学校可以公布论文（设计）的全部或部分内容。
保密的论文（设计）在解密后适用本规定。
作者签名：指导教师签名：日期：日期：毕业论文（设计）答辩委员会(答辩小组)成员名单摘要酶解法提取桉树叶中原花青素的工艺。
［方法］采用酶解法提取桉树叶中原花青素，在单因素试验的基础上，采用L16(45)正交试验设计，研究酶的浓度酶解温度酶解时间和料液比对桉树叶原花青素得率的影响。
［结果］在桉树叶原花青素得率的各影响因素中，影响程度依次为:料液比＞酶解浓度＞酶解时间＞酶解温度。
提取桉树叶原花青素的最佳工艺条件为:以0.5纤维素酶为提取溶剂，采用料液比为1∶50在50℃和酶解90min条件下原花青素得率为1.6722mg/g。
［结论］研究可为提高桉树利用率和工业化生产高附加值的原花青素提供数据。
关键词酶解法;桉树叶;原花青素;提取.ABSTRACTEnzymatic extraction process proanthocyandins eucalyptus leaves. [Method] The enzymatic extraction proanthocyandins eucalyptus leaves, on the basis of single factor test, using L16 (45) orthogonal design study of the concentration of enzyme hydrolysis time and hydrolysis temperature solid-liquid ratio of eucalyptus leaves proanthocyanidins yield Impact. [Result] various factors eucalyptus leaves procyanidins yield, the degree of impact as follows: solid-liquid ratio> enzyme concentration> reaction time> reaction temperature. The optimum conditions for extraction of eucalyptus leaves proanthocyanidins were as follows: 0.5 cellulase extraction solvent, the solid-liquid ratio of 1:50 at 50 ℃and hydrolysis 90min conditions proanthocyanidins yield 1.6722mg / g.[Conclusion] The study can provide data for improving eucalyptus utilization and industrial production of high value-added proanthocyanidins.Keywords: Enzymatic; eucalyptus leaves; proanthocyanidins; extraction.目录摘要 (4)ABSTRACT (5)1引言 (1)2 实验部分 (2)2.1 实验器材、药品 (2)2．2 方法 (2)2．2．1 原花青素最大吸收波长的选择 (2)2．2．2 原花青素含量计算。
花青素相关论文
Food and Chemical Toxicology 43 (2005) 1557–1566/locate/foodchemtoxE ects of anthocyanidin on the inhibition of proliferation andinduction of apoptosis in human gastric adenocarcinoma cellsPing-Hsiao Shih, Chi-Tai Yeh, Gow-Chin Yen *Department of Food Science, National Chung Hsing University, 250 Kuokuang Road, Taichung 40227, TaiwanReceived 15 December 2004; accepted 4 May 2005AbstractAnthocyanins are naturally occurring reddish pigments that abundant in fruits and vegetables. To investigate the mechanistic basis for the anti-tumor properties of anthocyanins, five aglycone (cyanidin, delphinidin, malvidin, pelargonidin, and peonidin) and four glycosylated (cyaniding-3-glucoside, malvidin-3-glucoside, pelargonidin-3-glucoside and peonidin-3-glucoside) anthocyanins were used to examine their e ects on cell cycle progression and induction of apoptosis in human gastric adenocarcinoma AGS cells. The data from cell viability assay showed that malvidin exhibited the most potent anti-proliferation e ect on AGS cells in a time-and dose-dependent manner (P < 0.05). This event is accompanied the arrest of AGS cells at the G0/G1 phase by malvidin at the tested concentrations of 0–200 lM. Cellular uptake of anthocyanin and anthocyanidin was confirmed by HPLC analysis and the intracellular accumulation of malvidin (24.9 ± 1.1 lM/mg protein) was observed when treatment of AGS cells with malvidin for 12 h. In addition, an accumulation of AGS cells in sub-G1 phase (20% and 30% increase for 100 and 200 lM of malvidin, respectively) was observed as well as by the appearance of a fraction of cells with an aneudiploid DNA content. The occurrence of apoptosis induced by malvidin was confirmed by morphological and biochemical features, including apoptotic bodies formation, caspase-3 acti-vation and poly(ADP-ribose) polymerase proteolysis. Furthermore, the mitochondrial membrane potential of apoptotic cells after treatment with malvidin was significantly lost and resulted in the elevation of Bax/Bcl-2 ratio for 1.6-fold against control for100lM treatment. In addition, the malvidin treatment significantly increased the p38 kinase expression and inhibited the ERK activ-ity, and the e ects of malvidin on caspase-3 activation were blocked, respectively, by the ERK and p38 inhibitors. These findingssuggest that growth inhibition and cytotoxicity of AGS cells by malvidin is involved in the induction of apoptosis rather than necrosis. 2005 Elsevier Ltd. All rights reserved.Keywords: Anthocyanidin; Apoptosis; AGS cells; MAPK pathway; Bcl-2 family1. IntroductionFollowing the change of dietary habits and the exces-sive process of food, the tendency of gastrointestinal dis-ease is on the rise. Gastric cancer is a kind of gastrointestinal (GI) tract cancer that is the leading cause of cancer-related mortality in the world and approximately 90% of stomach cancers are adenocarci-*Corresponding author. Tel.: +886 4 2287 9755; fax: +886 4 2285 4378.E-mail address: *****************.edu.tw (G.-C. Yen).0278-6915/$ - see front matter 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.fct.2005.05.001 nomas (Kelley and Duggan, 2003). Studies have shown that a high intake of smoked, salted, nitrated foods and carbohydrates, but a low intake of vegetables, fruits, and milks, are linked to cancer incidence. These diets have been shown to significantly increase the risk for stomach cancer (Serafini et al., 2002). Epidemiological studies have provided convincing evidence that dietary factors can modify the process of carcinogenesis, includ-ing initiation, promotion and progression of several types of human cancer (Ray, 2005). The occurrence of gastrointestinal (GI) cancers has increased strikingly during the past decade. Despite advances in early1558P.-H. Shih et al. / Food and Chemical Toxicology 43 (2005) 1557–1566diagnosis and treatment modalities, the side e ects of chemical drugs and recurrence are still the problems. Therefore, the development of chemotherapeutic/che-mopreventive agents for gastric cancer is important for reducing the mortality caused by this disease.Anthocyanins are glycosides of anthocyanidins univer-sally associated with attractive, colorful, and flavorful fruits. Recently, there has been a resurgence of interest in anthocyanins due to their potential biological and phar-macology benefit, such as: antioxidant (Moyer et al.,2002), anti-inflammatory (Subarnas and Wagner, 2000),reducing the risk of cardiovascular diseases (Wang and Mazza, 2002),and anti-tumor properties (Katsube et al., 2003). Animal studies have also demonstrated that feeding with anthocyanin-rich extract protected against tert-butyl hydroperoxide-induced hepatic toxicity (Wang et al.,2000) and decrease lipid peroxidation and DNA damage in vitamin E-depleted rats (Ramirez-Tortosa et al.,2001). More recently, anthocyanins have been shown to be an e ective chemopreventive agent against 1,2-dimethyhydrazine- and 2-amino-1-methyl-6-phenylimi-dazo[4,5-b]pyridine-induced mammary carcinogenesis in rats (Hagiwara et al., 2002). In addition, anthocyanins can be directly absorbed and distributed to the blood (Tsuda et al., 1999), and to be incorporated in cell cultures, both in the plasma membrane and in the cytosol (Youdim et al., 2000). Extensive studies indicate that anthocyanins have strong free radical scavenging and antioxidant activi-ties (Wang et al., 1997), suggesting that they play an important role in preventing against mutagenesis and car-cinogenesis (Omenn, 1995). Anthocyanins also showed inhibitory e ects on the growth of some cancer cells (Kamei et al., 1995). Our recent study has reported (Yeh and Yen, 2005) that the induction of apoptosis by the anthocyanidins through regulation of Bcl-2 gene and activation of c-jun n-terminal kinase cascade in hepatoma cells. However, the research concerning the protective e ect of anthocyanins against gastric adenocarcinoma is limited; thus, the objective of the present study was to determine whether anthocyanins would be useful in the prevention of human gastric adenocarcinoma car-cinogenesis. In the present study, human cultured gastric adenocarcinoma (AGS) cells were chosen for study.AGS cells line has been shown to grow in athymic mice and to have the same histochemical and cytological characteristics as the specimen taken from the patient. It is important to characterize human tumor cells in vitro in this detailed manner, since they serve as excellent model systems for other studies involving the heterogeneous re-sponses to anticancer drugs (Barranco et al., 1983), and recently this cell line has been widely used as a model sys-tem for evaluating cancer cell apoptosis (Liu et al., 2003).Apoptosis is a defined type of cell death and di ers from traditional cell death, necrosis. Many recent stud-ies have indicated that anticancer drugs or cancer che-mopreventive agents act through the induction of apoptosis to prevent tumor promotion, progression, and the occurrence of cellular inflammatory responses other than necrosis. Apoptosis is also a gene-directed form of cell death with well-characterized morpholo-gical and biochemical features (Brown and Attardi,2005). Initiation of apoptosis appears to be a common mechanism of many cytotoxic agents used in chemother-apy. Therefore, apoptosis inducing agents are expected to be ideal anticancer drugs. In addition, some flavo-noids, such as quercetin, apigenin, and phloretin, inhibit cancer cell growth through the induction of apoptosis (Wang et al., 1999). Therefore, understanding the mech-anism of apoptosis has important implications in the prevention and treatment of many diseases.In this study, we investigated the induction of apop-tosis by five typical anthocyanins and their relative antho-cyanidins in human gastric adenocarcinoma cells. In addition, the molecular mechanisms of the apoptotic e ects induced by malvidin were also determined.2. Materials and methods2.1. MaterialsAnthocyanidins [cyanidin chloride, delphinidin chloride, malvidin chloride, pelargonidin chloride, peonidin chloride], anthocyanins [cyanidin-3-O-gluco-side chloride, malvidin-3-O-glucoside chloride (oenin), pelargonidin-3-O-glucoside chloride, and peonidine-3-O-glucoside chloride] were obtained from Extrasynthese (Genay, France). Human adenocarcinoma AGS cells were purchased from the Bioresource Collection and Research Center (BCRC, Food Industry Research and Development Institute, Hsin Chu, Taiwan). Goat anti-rabbit IgG polyclonal antibody conjugated to peroxidase were obtained from Sigma Chemical Co. (St. Louis, MO, USA). Anti-ERK, anti-phospho-ERK, anti-JNK, anti-phospho-JNK, anti-p38, anti-phospho-p38, anti-capsase-3, anti-poly (ADP-ribose) polymerase, and anti-b-actin antibodies were obtained from Cell Signaling Technology (Beverly, MA). Anti-Bcl-2, and anti-Bax antibodies were obtained from Pharmingen (San Diego, CA). Molecular mass markers for proteins were obtained from Pharmacia Biotech (Saclay, France). Polyvinyldi-fluoride (PVDF) membrane for Western blotting was obtained from Millipore (Bedford, MA, USA).2.2. Cell cultureThe AGS cells were cultured in Ham s F-12K medium supplemented with 10% heat-inactivated fetal bovine serum (FBS) and antibiotics (100 U/ml penicillin,100lg/ml streptomycin) at 37 LC in a humidified atmo-sphere of 5% CO2. During the experiments the concen-tration of FBS were adjusted to 5%.P.-H. Shih et al. / Food and Chemical Toxicology 43 (2005) 1557–1566 15592.3. Cell morphological observationMorphology of control cells and samples-treated cells were detected by phase contrast microscope (Nicon).2.4. Cell viability assayCell viability assay was performed with MTT photo-metric analysis and trypan blue dye exclusion method. In the MTT assay, 5 ·104cells were seeded in 96-well microtiter plate. Cells were treated without or with va-rious concentrations of di erent samples. At the end of incubation, the supernatants were exchanged with90ll fresh medium and 10 ll of MTT (1 mg/ml) solu-tion. After 3 h incubated at 37 LC, aspirated the medium and dissolved the violet crystals with 100 ll of DMSO and the extent of the reduction of MTT was measured by ELISA reader.The cytotoxicity of anthocyanin and anthocyanidin was achieved through incubation of 2 · 105 cells in the 24-well culture plate untreated or treated with di erent samples. Cells were harvested and added 10 ll of trypan blue (0.4%). The dye exclusion method was performed by calculating the number of died cells over the control.2.5. Cell collection and HPLC analysis of intracellular anthocyanin and anthocyanidin contentFollowing incubation of anthocyanin and anthocy-anidin (500 lM) with AGS cells for 4, 8, 12 and 16 h, cells were washed twice with PBS and then the method for the determination of intracellular anthocyanin and anthocyanidin was followed with Kader et al. (1996)and Youdim et al. (2000). Cell pellets were resuspended with 10 ll of 1% Triton X-100 and 10 ll of 1 N HCl, vortexed vigorously and allowed to stand at 4 LC for 20 min. The HPLC analysis (Hitachi L-6200 intelligent pump equipped with a photodiode array detector Hit-achi L-7455) with a LiChroCART RP-18 reversed phase column (200 · 4 mm, 5 lm) and using the mobile phase consisting of water/formic acid (90:10, v/v) (solvent A) and water/acetonitrile/methanol/formic acid (40:22.5: 22.5:10, v/v) (solvent B). Initial starting conditions were 20% B, between 0 and 15 min % B increased from 20% to 25%, 15–60 min % B increased from 25% to 40%, 60–80 min % B increased from 40% to 80%, at 80 min mobile phases were switched to original starting condi-tions (20% B) and held at this condition for 10 min prior to the next injection.2.6. Flow cytometric analysisTo investigate the e ects of malvidin on the cell cycle distribution of AGS cells, cells (2 ·106cells/ml) treated with various concentrations of malvidin and cultured for 0–72 h were harvested, washed with phosphate-buf- fered saline and fixed in 75% of ethanol at 4 LC over-night. After washing twice with cold PBS, cells were resuspended in PBS containing 40 lg/ml propidium iodide (PI) and 0.1 mg/ml RNase followed with shaking at 37 LC for 15 min. Cells were analyzed with flow cytometer (Becton-Dickinson Immunocytometery Sys-tems, San Jose, CA) and the data were consequently evaluated by Cell Quest and Mod-Fit.2.7. Mitochondrial membrane potential (DWm)Mitochondrial membrane potential was analyzed with the J-aggregate forming lipophilic compound 5, 50, 6, 6 tetrachloro-1, 1, 3, 3 tetraethylbenzamidazolo-carbocyanin iodide (JC-1), which has been incorporated into the MitoPT TM kit (Serotec Inc., UK) that is repro-ducible detection of the mitochondrial permeability transition (PT) events in apoptotic cells. AGS cells (1 · 105 cells/ml) were seeded onto 96-well plate and treated with various concentrations of malvidin for indi-cated time followed by incubated the cells that stained with the MitoPT TM dye reagent at 37 LC for 15 min in the CO2incubator. The aggregate red form was detected by FLUO star galaxy spectrophotometer (BMG Lab-technologies Ltd., O enburg, Germany) after excitation at 485 nm and emission at 520 nm. The apoptotic cells were showed up the accumulation of green fluorescence compared with control.2.8. Measurement of caspase-3 activityFor the determination of caspase activity, the down-stream executor enzyme caspase-3 was evaluated. Cells were pretreated with various doses of ERK and p38 inhibitors, respectively, for 1 h, and following the treat-ment of malvidin (100 lM) for 48 h. At the end, the cas-pase-3 activity was measured by proteolytic cleavage of the fluorogenic substrate using the CaspaTagTM Cas-pase-3 (DEVD) Activity kit (BioTech Inc., USA). Cells (1 ·106 cells/ml) from di erent treatments were col-lected and incubated with the Working Dilution reagent at 37 LC for 1 h, and after washing with the wash bu er, the cells were resuspended with PBS and the fluorescent intensity was detected by the fluorescence spectropho-tometer with the excitation wavelength of 485 nm and the emission wavelength of 520 nm.2.9. Western blotThe cytosolic proteins were isolated from AGS cells (2 · 106 cells/ml) after treatment with 100 lM malvidin for various times. The total proteins were extracted by adding 800 lL of cold lysis bu er (50 mM Tris–HCl, pH 7.4; 1 mM NaF; 150 mM NaCl; 1 mM EGTA; 1 mM phenylmethylesulfonyl fluoride; 1% NP-40; and 10 lg/ml leupeptin) to the cell pellets on ice for1560P.-H. Shih et al. / Food and Chemical Toxicology 43 (2005) 1557–156630 min, followed by centrifugation at 12,000 · rpm for 10 min at 4 LC. The supernatant protein concentration was measured by Bio-Rad DC kit with bovine serum albumin (BSA) as the standard. The cell lysate were mixed with 4 · sample bu er (8% SDS; 0.04% coomassie blue R-250; 40% glycerol; 200 mM Tris, pH 6.8 and 10% 2-mercaptoethanol) and boiled for 10 min. SamplesTable 1E ect of anthocyanins and anthocyanidins on human gastric adeno-carcinoma cell AGS viabilitySamples (200 lM) Cell viability(% of control)a Cyanidin 78 ± 1.3Cyanidin-3-glucose 83 ± 2.4Peonidin 89 ± 1.1Peonidin-3-glucose 84 ± 0.9Pelargonidin 86 ± 3.1Pelargonidin-3-glucose 81 ± 0.8Malvidin 63 ± 1.1Malvidin-3-glucose (oenin) 69 ± 2.3Delphinidin 67 ± 0.9a Cells were treated with 200 lM of nine samples for 48 h. The cell viability assay was determined by MTT assay. Data are as the mean ± SDof three independent experiments.were electrophoresed in a 10% SDS-PAGE minigel and then transferred onto polyvinylidenedifluoride membranes (PVDF; Millipore Corp., Bedford, MA)100control)80DelphinidinOeninMalvidinof60(%viability40Cell200 50 100 150 200 250Concentration ( M)Fig. 1. Inhibition of AGS cells viability by anthocyanin and antho-cyanidin. AGS cells were treated with various concentrations of three samples for 48 h. After treatment, cell viability was estimated by trypan blue dye exclusion method. Data are the mean ± SD of three independent experiments.Fig. 2. HPLC determination of anthocyanin and anthocyanidin incorporated into AGS cells. Data are presented from three independent experiments.P.-H. Shih et al. / Food and Chemical Toxicology 43 (2005) 1557–1566 1561with transfer bu er (48 mM Tris; 39 mM glycine; 0.0037% SDS and 20% methanol) at 350 mA for 60 min. The membranes were blocked with 5% nonfat milk in PBS solution containing 0.1% Tween-20 (PBST) for 1 h. The membrane was immunoblotted with pri-mary antibodies of rabbit anti-human caspase-3, PARP, Bcl-2 family and MAPK family in PBS solution that contained 5% BSA in overnight at 4 LC. After consecu-tively washed with PBST for 30 min, the membrane was incubated with horseradish peroxidase-labeled second-ary antibody for 60 min at room temperature and washed with PBST for 30 min. Final detection was per-formed with enhance chemiluminescence (ECL TM kit) western blotting reagents (Amersham Pharmacia Bio-tech, New Jersey, USA). 2.10. Statistical analysisAll data are presented as means ±SD. The statistical significant di erences compared with untreated group were calculated by Duncan s multiple range test.3. Results3.1. E ect of anthocyanins and anthocyanindins onthe cell viability of human gastric adenocarcinoma AGS cellsIn preliminary experiments, the e ects of four antho-cyanins and five anthocyanidins on the proliferation ofFig. 3. Interruption of cell cycle in malvidin-treated AGS cells for 24 h. (A) The cell morphology and the cell cycle distribution by flow cytometric determination. (B) Significant accumulation at G0/G1 phase both 100 and 200 lM of malvidin-treated cells that compared with control (*p < 0.05).1562P.-H. Shih et al. / Food and Chemical Toxicology 43 (2005) 1557–1566AGS gastric adenocarcinoma cells were evaluated. The proliferation assay was performed by MTT assay, and found that malvidin, delphinidin, and malvidin-3-glucoside (oenin) showed much e cacy of anti-cell pro-liferation abilities (Table 1). In view of the potential anti-tumor abilities of these compounds, the cell viabil-ity was further evaluated by trypan blue dye exclusion assay, the result is shown in Fig. 1. The IC50 value of delphinidin, oenin and malvidin was 198, 149 and 128 lM, respectively, for 48 h incubation.To evaluate the bioavailability of anthocyanin and anthocyanidin, the cytosolic concentrations of delphini-din, oenin and malvidin were detected by HPLC method. As shown in Fig. 2, the incorporation of those three samples into AGS was very quickly and reached the limitation within 12 h. The cytoplasmic concentrations of those three samples, expressed in lM/mg protein, ranged from 25.1 for oenin to 16.4 for malvidin.3.2. Apoptosis induction of AGS cells by malvidinAs the results shown in Fig. 3A, the classical apopto-tic cells were observed in malvidin-mediated cell death from cell shrinkage and membrane blabbing to the for-mation of apoptotic bodies. In comparison with the con-trol, malvidin treatment significantly accumulated the percentage of cells at G0/G1 phase (Fig. 3B) for 24 h of incubation (74% and 79% under 100 and 200 lM treatment, respectively). Interestingly, the sub-G1 phase of cells were significantly increased from 3% to 20% and 33% under 100 and 200 lM malvidin treatment for 48 h, respectively, and in a time and dose dependent manner (as shown in Fig. 4A and B). Further more, the enzy-matic activation of caspase-3 was evident within 50–200lM malvidin treatment, and similar characteristics of proteolytic PARP protein were also detected by wes-tern blotting in AGS cells treated for 48 h with 100–200lM of malvidin (Fig. 4C).3.3. E ect of malvidin on the mitochondrial stability of AGS cellsTo further define the feature of malvidin-induced apoptosis in AGS cells, the mitochondrial membrane potential of AGS cells was detected. This was performed by using the MitoPT TM kit, which specific detects the apoptotic feature in the early phase. Fig. 5A shows that 100lM of malvidin induced serious mitochondrial dis-ruption after 24 h incubation (69.5% of total cells). The Bcl-2 family of pro- and anti-apoptotic proteins expression of AGS cells was further analyzed and found that the elevation of Bax/Bcl-2 ratio for 1.6- and 2.1-fold against control for 100 and 200 lM treatments (Fig. 5B and C). These data demonstrated an apoptotic e ect of malvidin in AGS cells.Fig. 4. Malvidin-induced apoptosis in AGS cells. (A) Cells were treated with 100 lM of malvidin for indicated time. (B) Cells were treated with 50, 100 and 200 lM malvidin for 48 h. The data was calculated by using FACScan software. All data represent the mean ±SD of three independent experiments. Asterisks indicate significant di erence by comparison with control as determined by Duncan s multiple range test, *p < 0.05; **p < 0.001. (C) Representative western blotting of caspase-3 activation and PARP proteolytic fragment in AGS cells by treated with di erent concentrations of malvidin for 48 h.P.-H. Shih et al. / Food and Chemical Toxicology 43 (2005) 1557–1566 1563 Fig. 5. The changes of mitochondrial membrane potential in AGS cells undergoing malvidin-induced apoptosis. (A) AGS cells were pretreated with100lM of malvidin for di erent time. (B) Western blotting analysis of Bcl-2 family of AGS cells by 100 and 200 lM malvidin treatments for 24 h. Histograms show densitometric analysis of protein expression. Data are the mean ± SD of three independent experiments.3.4. Involvement of the MAP-kinases p38 and ERK in malvidin-induced apoptosisSince MAPK pathways involved the growth and death of the cell, the changes of phospho-JNK, ERK and p38 protein levels in the AGS cells treated with mal-vidin were examined by western blotting technique. As shown in Fig. 6, cells were exposed to 100 lM of malvi-din and the level of phospho-ERK protein was reduced to 55% for 48 h incubation (Fig. 6A), and the expression of phospho-p38 protein showed a significant 2.3-fold in-crease for 36 h incubation as compared to the control (Fig. 6B). However, there was no significant di erence in the expression of phospho-JNK levels (data not shown). Furthermore, the specific inhibitors were used to determine of the exact molecular mechanisms of mal-vidin-induced apoptosis through MAPK pathway. The data showed that treatment of AGS cells with malvidin (100 lM) induced a significant increase of the activity of caspase-3, and pre-incubation of cells with the ERK inhibitor PD98059 (40 lM) synergistically promoted the e ect of malvidin. While pretreatment with p38 inhibitor SB203580 (50 lM) abrogated the e ect of mal-vidin on caspase-3 activation. 4. DiscussionAmong the nine kinds of anthocyanins and anthocy-anidins studied in the present study, malvidin had more e ciency in anti-proliferation and cytotoxicity of AGS cells with a time- and dose-dependent manner. Thus, the molecular mechanisms of the apoptotic e ects in-duced by malvidin were further evaluated. Some studies of the induction of apoptosis by malvidin in di erent tumor cell lines have been reported, including the medi-ation of programmed cell death in human promyelocytic leukemia cells (Katsube et al., 2003) and the arrest of cell cycle progression in human monocytic leukemia cells (Hyun and Chung, 2004). Although there are some studies of the bioavailability of anthocyanins in human (Matsumoto et al., 2001; McGhie et al., 2003) and animal models (Tsuda et al., 1999), this is the first study reported that the uptake of anthocyanins in human gas-tric cells. The stomach is a good organ for the stabiliza-tion of anthocyanins because of its acidic environment (Passamonti et al., 2003). The data showed that the maximum incorporation of anthocyanin and anthocy-anidin into AGS cells was reached a maximum after 12 h of incubation (Fig. 2). Recently, Passamonti et al.1564P.-H. Shih et al. / Food and Chemical Toxicology 43 (2005) 1557–1566Fig. 6. E ect of malvidin on the expression of MAPK family and caspase-3 activity in AGS cells. Cells were treated with 100 lM of malvidin for indicated time and the western blotted to reveal the expression of (A) phopho-ERK, (B) phospho-p38, and (C) caspase-3 activity treated with or without MAPK inhibitors for 48 h. Similar results were obtained in three independent experiments. *p < 0.05 versus control; #p < 0.01 versus malvidin.(2002) had compared the bioavailability of some samples including delphinidin, malvidin and malvidin-3-O-glucoside (oenin). The incorporation of anthocya-nin into AGS cells was detected by HPLC followed the method of Kader et al. (1996) with a slight modifica-tion. In addition, there are still other methods for anal-ysis of anthocyanins and anthocyanidins in lots of di erent vegetables and fruits (Merken and Beecher,2000).Nyman and Kumpulainen (2001) and Zhang et al. (2004) showed that the retention time of malvidin was latter than delphinidin, cyanidin and other anthocy-anidins. These data showed that oenin possesses the best bioavailability than others due to its best e cacy of binding to organic anion membrane carrier, bilitranslocase.Gastric cancer is the second most common cause of cancer-related mortality in the world and the therapies such as surgical operation or radiotherapy at later stages may incur a poor prognosis with overall 5-year survival rates of less than 25% (Houghton et al., 2002). Lately the treatment for gastric prefer to the chemotherapy that intensive treatment of anti-cancer curatives (Cascinu et al., 2004)or the genetic engineering that inhibition the proliferation and di erentiation of cancer cells (Steele and Lane, 2000; Heideman et al., 2004). Our strategy is to evaluate the biological functions of naturally occur-ring flavonoids, especially for anthocyanins, whether they have the potent ability to induce a programmed cell death in gastric carcinoma cells. In the present study, the morphological damages of classical apoptotic cells wereP.-H. Shih et al. / Food and Chemical Toxicology 43 (2005) 1557–1566 1565observed in malvidin-mediated cell death from cell shrinkage and membrane blabbing to the formation of apoptotic bodies (Fig. 3A). In comparison of the con-trol, malvidin treatment significantly accumulated the percentage of cells at G0/G1 phase (Fig. 3B) for 24 h of incubation; and further increased the number of sub-G1 cells, that was accompanied with activating the caspase-3 expression which resulted in the proteolysis of PARP (Fig. 4C). The results show that malvidin fur-ther a ects cells proliferation by arrest cell cycle progres-sion and sequentially induces apoptosis. Liu et al. (2004)also reported the similar results on the induction of apoptosis by lycorine on HL-cells.The mitochondrial dysfunction is associated with the intrinsic pathway of apoptosis (Desagher and Martinou, 2000; Ly et al., 2003). Bcl-2 family members were classi-fied into two major roles, one is the pro-apoptotic and the other is anti-apoptotic function (Kelekar and Thompson, 1998). When the death signal has been taken over, the C-terminal signal anchor sequences will target them to the outer membrane of organelles included mitochondria and then shift the permeability of mito-chondria. Our data showed that malvidin mediated the continued reduction of mitochondrial membrane poten-tial following with the incubation time (Fig. 5A), and elevated the ratio of Bax/Bcl-2 expression in a dose-dependent manner (Fig. 5B and C), which represented the pro/anti-apoptotic functions, respectively.Mitogen-activated protein kinases (MAPKs) family are well known of involving in the regulation of survival, proliferation and death of the cell (Johnson and Lapa-dat, 2002; Dent et al., 2003). In the present study, mal-vidin treatment had a profound e ect in the expression of the subfamilies of MAPKs, consist of ERK and p38 kinase. The data showed that malvidin could persis-tently decrease the activities of ERK (Fig. 6A), which responsible for the regulation of meiosis, mitosis and post-mitotic functions in cells (Johnson and Lapadat,2002),and then leaded to the anti-proliferation a ect.It has been reported that malvidin mediated the activa-tion of p38 enzyme expression, which is involved in apoptosis (Iwama et al., 2001). As shown in Fig. 6B, malvidin treatment revealed that the expression of p38 kinase seemed more activated than vehicle control. There are several specific inhibitors that are used for evaluating the exactly molecular mechanism. PD98059 specifically binds to MKK1/2, the ERK upstream ki-nases, and then inhibits ERK phosphorylation and acti-vation (Chuang et al., 2000). Previous studies have shown an inhibitory e ect of the p38 inhibitor SB 203580 on the DNA level (Diep et al., 2000; Yilmaz et al., 2003). In the present study, the data showed that p38 inhibitor SB203580 abrogates malvidin-induced expression of caspase-3, while ERK inhibitor PD98059 inhibits the stimulatory e ect of malvidin on caspase-3 activity. These data indicate the malvidin mediates the apoptosis of AGS cells is through the e ect of pro-and anti-apoptotic molecules of the MAPK family.Based on the results of this study, malvidin has a much e cacy than other samples tested on the induction of the programmed cell death in human gastric adeno-carcinoma AGS cells. The molecular mechanisms are due to the loss of mitochondrial membrane permeability and through the MAPK pathway. Therefore, anthocy-anidin should be good naturally occurring neutraceuti-cals for cancer preventions.AcknowledgmentThis work was supported by National Science Coun-cil Grant (NSC-92-2321-B005-006), Taiwan, Republic of China.ReferencesBarranco, S.C., Townsend Jr., C.M., Casartelli, C., Macik, B.G., Burger, N.L., Boerwinkle, W.R., Gourley, W.K., 1983. Establish-ment and characterization of an in vitro model system for human adenocarcinoma of the stomach. Cancer Research 43, 1703–1709. Brown, J.M., Attardi, L.D., 2005. The role of apoptosis in cancer development and treatment response. Nature Reviews of Cancer 5, 231–237.Cascinu, S., Scartozzi, M., Labianca, R., Catalano, V., Silva, R.R., Barni, S., Zaniboni, A., D Angelo, A., Salvagni, S., Martignoni, G., Beretta,G.D., Graziano, F., Berardi, R., Franciosi, V., 2004. High curativeresection rate with weekly cisplatin, 5-fluorouracil, epidoxorubicin, 6S-leucovorin, glutathione, and filgastrim in patients with locally advanced, unresectable gastric cancer: a report from the Italian Group for the Study of Digestive Tract Cancer (GISCAD). British Journal of Cancer 90, 1521–1525.Chuang, S.M., Liou, G.Y., Yang, J.L., 2000. Activation of JNK, p38 and ERK mitogen-activated protein kinases by chromium(VI) is mediated through oxidative stress but does not a ect cytotoxicity. Carcinogenesis 21, 1491–1500.Dent, P., Yacoub, A., Fisher, P.B., Hagan, M.P., Grant, S., 2003. MAPK pathways in radiation responses. Oncogene 22, 5885– 5896.Desagher, S., Martinou, J.C., 2000. Mitochondria as the central control point of apoptosis. Trends in Cell Biology 10, 369–377.Diep, Q.N., Touyz, R.M., Schi rin, E.L., 2000. Docosahexaenoic acid, a peroxisome proliferator-activated receptor-a ligand, induces apoptosis in vascular smooth muscle cells by stimulation of p38 mitogen-activated protein kinase. Hypertension 36, 851–855.Hagiwara, A., Yoshino, H., Ichihara, T., Kawabe, M., Tamano, S., Aoki,H., Koda, T., Nakamura, M., Imaida, K., Ito, N., Shirai, T., 2002.Prevention by natural food anthocyanins, purple sweet potato color and red cabbage color, of 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP)-associated colorectal carci-nogenesis in rats initiated with 1,2-dimethylhydrazine. The Journal of Toxicological Sciences 27, 57–68.Heideman, D.A., van Beusechem, V.W., Bloemena, E., 2004. Sup-pression of tumor growth, invasion and angiogenesis of human gastric cancer by adenovirus-mediated expression of NK4. The Journal of Gene Medicine 6, 317–327.Houghton, J., Fox, J.G., Wang, T.C., 2002. Gastric cancer: laboratory bench to clinic. Journal of Gastroenterology and Hepatology 17, 495–502.。
《基于花青素的智能食品包装薄膜的制备与性能研究》范文
《基于花青素的智能食品包装薄膜的制备与性能研究》篇一一、引言随着科技的发展和人们生活品质的提高，食品包装不仅需要满足基本的保护和保鲜功能，还需具有智能化、环保化的特点。
近年来，利用天然植物色素花青素作为原材料，研发制备出新型的智能食品包装薄膜，已经成为包装材料领域的研究热点。
本文以花青素为原料，探讨了智能食品包装薄膜的制备方法及其性能研究。
二、花青素与智能食品包装薄膜花青素，作为一种天然色素，具有抗氧化、抗衰老等生物活性，且来源广泛，如黑米、蓝莓、紫薯等。
将花青素应用于食品包装薄膜中，不仅可以为包装提供颜色和美感，还因其独特的生物活性对食品的保鲜、防氧化等方面有显著效果。
同时，这种以天然原料为基础的智能食品包装薄膜还具备环保可持续性。
三、制备方法（一）材料准备首先，需要收集含有花青素的植物材料，如黑米、蓝莓等。
然后通过提取、分离等工艺得到纯度较高的花青素。
同时，准备其他所需原料如聚乙烯醇、增塑剂等。
（二）制备过程将提取的花青素与聚乙烯醇等原料进行混合，通过搅拌、加热等工艺使原料充分融合。
然后通过流延法或熔融挤出法等方法将混合物制备成薄膜。
最后，进行干燥、热处理等后处理工艺，使薄膜达到所需的性能指标。
四、性能研究（一）机械性能通过对薄膜进行拉伸试验、冲击试验等测试手段，研究花青素含量、原料配比等因素对薄膜机械性能的影响。
结果表明，适量的花青素可以提高薄膜的机械强度和韧性。
（二）阻隔性能通过测定薄膜的透光性、氧气透过率、水蒸气透过率等指标，研究花青素智能食品包装薄膜的阻隔性能。
结果表明，该薄膜具有良好的阻隔性能，能有效保护食品免受外界环境的影响。
（三）生物活性及抗菌性能利用花青素的抗氧化、抗衰老等生物活性，研究其在包装薄膜中的应用效果。
同时，通过实验测定薄膜的抗菌性能，探讨其在延长食品保质期方面的应用潜力。
结果表明，花青素智能食品包装薄膜具有显著的生物活性和抗菌性能。
五、结论本文以花青素为原料，研究了智能食品包装薄膜的制备方法及性能。
《基于花青素的智能食品包装薄膜的制备与性能研究》范文
《基于花青素的智能食品包装薄膜的制备与性能研究》篇一一、引言随着人们对食品安全与健康生活的关注度日益提高，智能食品包装材料的发展显得尤为重要。
花青素作为一种天然的、具有多种生物活性的物质，其应用在智能食品包装薄膜的制备中，不仅可以提高包装的功能性，还能为食品提供更好的保护。
本文旨在研究基于花青素的智能食品包装薄膜的制备方法及其性能，以期为相关领域的研究与应用提供理论支持。
二、花青素概述花青素是一种天然的色素，广泛存在于植物中，具有抗氧化、抗炎、抗癌等多种生物活性。
其结构特殊，能够与多种物质发生相互作用，因此在食品、医药、化妆品等领域具有广泛的应用。
将花青素应用于智能食品包装薄膜的制备中，不仅可以提高薄膜的抗氧化性能，还能为其赋予更多的智能特性。
三、制备方法基于花青素的智能食品包装薄膜的制备方法主要包括以下几个步骤：1. 材料选择：选择合适的花青素原料、聚合物基材以及其他添加剂。
2. 溶液制备：将花青素、聚合物基材及其他添加剂溶于适当的溶剂中，制备成均匀的溶液。
3. 薄膜制备：采用适当的成膜技术，如溶剂挥发法、相分离法等，将溶液转化为薄膜。
4. 性能优化：通过调整花青素含量、聚合物种类、添加剂种类及含量等参数，优化薄膜的性能。
四、性能研究基于花青素的智能食品包装薄膜的性能研究主要包括以下几个方面：1. 机械性能：通过拉伸试验、撕裂强度试验等手段，评价薄膜的机械性能。
2. 阻隔性能：测试薄膜对水分、氧气、油脂等物质的阻隔性能，以评估其保护食品的能力。
3. 抗氧化性能：通过DPPH自由基清除率、ABTS自由基清除率等指标，评价薄膜的抗氧化性能。
4. 智能特性：研究薄膜在温度、湿度、光照等条件下的响应性能，以及其在食品保鲜、防伪等方面的应用潜力。
五、结果与讨论通过实验研究，我们得到了以下结果：1. 制备得到的智能食品包装薄膜具有较好的机械性能和阻隔性能，能够满足食品包装的基本要求。
2. 薄膜中的花青素能够有效地清除DPPH和ABTS自由基，表现出较强的抗氧化性能。
小学生科技小论文：会变色的萝卜皮
会变色的萝卜皮南浔锦绣实验学校 602班沈通指导老师：韩晓鸣今天早晨，妈妈买回来几个红萝卜（红皮萝卜），呈鲜艳的紫红色。
她把一个红萝卜的皮削下来，扔在洗过手套的肥皂水中。
中午，我发现皮的颜色不再是鲜艳的紫红色，而是偏蓝色了。
这是怎么回事呢？于是我尽力猜想可能的原因：一、可能是像切开的苹果一样，被氧化后就变蓝色了；二、可能是红萝卜皮浸在水中会变蓝；三、可能是红萝卜皮中的某物质与肥皂中的物质相互作用而变蓝色的。
为了得知自己的猜想是否正确，我将一个红萝卜的皮削下来，分成三份。
一份放在桌上，一份浸在清水中，还有一份浸在新配制的肥皂水中。
过了大约半小时，我发现只有放在肥皂水中的有点变蓝。
再过一小时左右，发现浸在肥皂水中的变蓝色更明显了，而其他两份仍然是鲜艳的紫红色。
由此可知，猜想一和猜想二都是错误的，猜想三是正确的。
紧接着，我又有了新的疑问：红萝卜皮中到底含有什么物质而让它呈紫红色了？这种物质在肥皂水中为什么会变蓝？这种物质遇到别的物质还会变成其他颜色吗？带着疑问，我到互联网上去查找资料。
查到的相关资料是：红萝卜皮中含有一种叫花青素的物质，所以呈紫红色。
花青素又称花色素，是一种天然色素，花卉、水果、蔬菜的颜色大部分与之有关。
花色素的颜色会随着身处环境的酸碱性不同而有所变化，在酸性条件下呈红色或紫色，在碱性条件下呈蓝色。
我回想起爸爸曾经跟我用pH试纸测试过，石灰水是呈强碱性的，并告诉我肥皂水、牙膏等是弱碱性的，我也知道家里的食醋是酸性的。
为了验证萝卜皮中色素的颜色变化情况是否与资料中所述情况一样，我又进行了以下实验：1.用海苔包装中的干燥剂（生石灰）配制好石灰水，并准备好白醋。
2.将红萝卜皮捣碎，榨出紫红色的汁液分成三份。
第一份中加入少量石灰水，很快变蓝色；第二份中加入少量白醋，颜色从紫红变得更偏向红色了；第三份加入少量清水后颜色基本不变，只是紫红色变浅些。
这些现象与互联网资料中所述情况相符合，这让我感到非常兴奋。
花青素 作文
花青素作文
《神奇的花青素》
嘿，你们知道吗？有一种特别神奇的东西叫花青素！
花青素就像是一个会变魔法的小精灵。
在不同的环境下，它能变出各种不一样的颜色呢！
我第一次知道花青素是在妈妈给我讲的故事里。
妈妈说，花青素藏在好多好多的植物里面，比如葡萄呀、蓝莓呀、紫薯呀。
我特别好奇，花青素到底长什么样子呢？它怎么就能变色呢？
有一次，我们上科学课的时候，老师给我们做了一个实验，就是用紫甘蓝汁来测试不同的液体。
哇，我看到紫甘蓝汁遇到不同的东西，颜色真的变了呢！有时候变成了红色，有时候变成了蓝色，简直太神奇啦！
后来我才知道，原来花青素会根据环境的酸碱度来改变颜色。
酸一点的时候，它可能就变成红色；碱一点的时候，它可能就变成蓝色或者绿色。
花青素可太有意思啦！我觉得它就像是大自然给我们的一份神秘礼物。
我好想继续去探索花青素的秘密呀，说不定还有更多好玩的事情等着我去发现呢！我真希望我能快点长大，然后懂得更多关于花青素的知识。
花青素实验作文范文
花青素实验作文范文
哇，这花瓣颜色真靓啊，像紫宝石一样闪闪发光。
凑近点看，发现上面有些小颗粒，是不是就是传说中的花青素啊？这玩意儿也太神奇了吧，能让花变得这么好看。
做实验的时候，我把花瓣放进试管里，滴了几滴溶剂，然后就看到花瓣变得有点白了。
但试管里的液体开始变色了，深紫色，超级好看！我就在想，这花青素是不是就像变色龙一样，换个环境就换个颜色啊？
“你看这个，这就是花青素的作用。
”老师指着试管里的液体说。
他解释了一大堆关于花青素怎么和溶剂反应，怎么在细胞里起作用。
听得我一愣一愣的，感觉自己好像打开了新世界的大门。
原来这小小的花青素，还有这么多学问呢！
走出实验室，天都黑了。
我走在路上，突然又想起那深紫色的液体。
突然觉得，花青素这东西，真的就像是大自然的魔法一样。
每次做实验，都像是在和这魔法打交道，真是让人兴奋啊！。
花青素 作文
花青素作文
哎呀，花青素可真是一种神奇的东西！
嘿嘿，我第一次听说花青素是在科学课上，老师告诉我们，花青素是一种天然的色素，它可以让植物的花朵、果实和叶子变得五颜六色。
哈哈，我觉得花青素就像一个魔法师，它可以把平淡无奇的植物变得美丽动人。
我还知道，花青素不仅可以让植物变得漂亮，还对我们的身体有很多好处呢！
哎呀，比如说，花青素可以抗氧化，预防癌症和心脏病；它还可以保护我们的眼睛，让我们的视力更好。
嘿呀，所以，我觉得花青素真的很了不起！我要多吃一些含有花青素的食物，比如蓝莓、紫薯、葡萄等等，让自己变得更健康！。
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2015年度本科生毕业论文（设计）桉树叶中原花青素的提取英文题目Extraction of anthocyanins fromleaves of Eucalyptus院（系）：资源环境学院专业：化学年级： 2012级学生姓名：王兴刊学号： 120640135导师及职称：张星和（助教）2015年 06月毕业论文（设计）原创性声明本人所呈交的毕业论文（设计）是我在导师的指导下进行的研究工作及取得的研究成果。
据我所知，除文中已经注明引用的内容外，本论文（设计）不包含其他个人已经发表或撰写过的研究成果。
对本论文（设计）的研究做出重要贡献的个人和集体，均已在文中作了明确说明并表示谢意。
作者签名：日期：毕业论文（设计）授权使用说明本论文（设计）作者完全了解保山学院有关保留、使用毕业论文（设计）的规定，学校有权保留论文（设计）并向相关部门送交论文（设计）的电子版和纸质版。
有权将论文（设计）用于非赢利目的的少量复制并允许论文（设计）进入学校图书馆被查阅。
学校可以公布论文（设计）的全部或部分内容。
保密的论文（设计）在解密后适用本规定。
作者签名：指导教师签名：日期：日期：毕业论文（设计）答辩委员会(答辩小组)成员名单摘要酶解法提取桉树叶中原花青素的工艺。
［方法］采用酶解法提取桉树叶中原花青素，在单因素试验的基础上，采用L16(45)正交试验设计，研究酶的浓度酶解温度酶解时间和料液比对桉树叶原花青素得率的影响。
［结果］在桉树叶原花青素得率的各影响因素中，影响程度依次为:料液比＞酶解浓度＞酶解时间＞酶解温度。
提取桉树叶原花青素的最佳工艺条件为:以0.5纤维素酶为提取溶剂，采用料液比为1∶50在50℃和酶解90min条件下原花青素得率为1.6722mg/g。
［结论］研究可为提高桉树利用率和工业化生产高附加值的原花青素提供数据。
关键词酶解法;桉树叶;原花青素;提取.ABSTRACTEnzymatic extraction process proanthocyandins eucalyptus leaves. [Method] The enzymatic extraction proanthocyandins eucalyptus leaves, on the basis of single factor test, using L16 (45) orthogonal design study of the concentration of enzyme hydrolysis time and hydrolysis temperature solid-liquid ratio of eucalyptus leaves proanthocyanidins yield Impact. [Result] various factors eucalyptus leaves procyanidins yield, the degree of impact as follows: solid-liquid ratio> enzyme concentration> reaction time> reaction temperature. The optimum conditions for extraction of eucalyptus leaves proanthocyanidins were as follows: 0.5 cellulase extraction solvent, the solid-liquid ratio of 1:50 at 50 ℃and hydrolysis 90min conditions proanthocyanidins yield 1.6722mg / g.[Conclusion] The study can provide data for improving eucalyptus utilization and industrial production of high value-added proanthocyanidins.Keywords: Enzymatic; eucalyptus leaves; proanthocyanidins; extraction.目录摘要 (4)ABSTRACT (5)1引言 (1)2 实验部分 (2)2.1 实验器材、药品 (2)2．2 方法 (2)2．2．1 原花青素最大吸收波长的选择 (2)2．2．2 原花青素含量计算。
公式如下： (2)2．2．3 单因素试验 (2)2．2．3．1 酶的浓度对原花青素得率的影响 (2)2．2．3．2 酶解温度对原花青素得率的影响 (3)2．2．3．3 酶解时间对原花青素得率的影响 (3)2．2．3．4 料液比对原花青素得率的影响 (3)2．2．4正交试验设计 (3)2.2.5原花青素含量的测定 (4)3 结果与分析 (4)3．1 原花青素紫外可见分光光度计扫描结果 (4)3．2 桉树叶原花青素提取单因素试验 (5)3．2．1 酶的浓度对原花青素得率的影响 (5)3．2．2 酶解时间对原花青素得率的影响 (5)3．2．3 酶解温度对原花青素得率的影响 (6)3．2．4 料液比对原花青素得率的影响 (6)4正交试验结果 (7)5结论 (8)参考文献 (9)致谢 (10)1引言原花青素 ( Procyanidins，PC)是植物中广泛存在的一大类天然多酚化合物的总称，它是由不同数量的儿茶素或表儿茶素缩合而成［1］现代研究表明，原花青素具有抗氧化［2］清除氧自由基［3］抗肿瘤［4］保护心脑血管和预防高血压［5］抗炎［6］抗诱变［7］等多种药理活性作用。
目前，原花青素广泛应用于保健食品药品和化妆品领域［2］。
因此该技术广泛应用于大分子生物活性物质的提取桉树叶有着很好的营养价值和特殊的保健作用［8］，桉树叶黄酮是包裹在细胞壁中，而这些细胞壁的主要成分是纤维素。
为了提高提率就必须先打破细胞壁释放出里面的物质。
所以纤维素就成了影响提取率的最大因素[9]。
为了避免有机溶剂的残留以及提高提取率，就要加入纤维素酶，破换细胞壁，让原花青素充分流出来。
据文献报道，桉树叶含有大量有效成分，这些物质具有强烈的生理活性，在食品、化工、医药、环境、能源等方面有着广泛的用途[10]。
我国的桉树资源十分丰富目前，如果从桉树叶中提取其有效成分，既综合利用了资源，加了桉树产业的附加值，又减少了环境的污染，具有一定的经济意义和价值，而有关桉树叶中原花青素提取的研究国内外报道甚少笔者通过正交试验优化桉树叶中原花青素的提取工艺条件，为提桉树叶的利用率和工业化生产高附加值的原花青素提供理论依据。
就目前利用原花青素的现状来看，只有在国外发达的国家应用比较广泛。
由于其技术水平有限和经济方面等各种因素的决定，导致原花青素的利用还比较局限。
但在发达地区原花青素已经被广泛的用与保健食品、医药及化妆品领域[6]。
在不久的将来，我国再利用原花青素的领域也将会更加深入，在法国，用葡萄仔提取的原花青素被制成了很多化妆品及用于眼睛疾病的治疗，还有淋巴功能不全及毛细管通透性疾病。
1990年日本Yanmaskosh研制了原花青素含量为1﹪的低聚体化合物，可使人体皮肤洁亮和美白其效果好于油性化妆品等其他美白系列产品[7]。
桉树叶中原花青素的提取2 实验部分2.1 实验器材、药品选材地:桉树叶，学校后山就地取材桉树叶晒干粉碎备用主要试剂: 无水乙醇、甲醇、正丁醇、盐酸、硫酸铁铵（以上化学试剂均为分析纯）。
主要仪器设备:电子天平，7230G可见分光光度计， HH-4型数显恒温水浴锅，GZX-9070MBE数显鼓风干燥箱，粉碎机。
2．2 方法2．2．1 原花青素最大吸收波长的选择准确移取1.0ml标准储备液于10mL比色管中，再加入6．0mL正丁醇－盐酸溶液( 95/5，V/V)和0．2mL,2%硫酸铁铵溶液，摇匀后，置沸水浴95℃（±5℃）加热40min，然后迅速冷却，将反应液用紫外可见分光光度计扫描，以确定最大吸收波长。
2．2．2 原花青素含量计算。
公式如下：得率=（C×V×N）/（1000W）×100% (2—1)式中，V，试样定容体积( mL) ; C，试样中原花青素浓度( mg/mL) ;N，稀释倍数;W，试样质量( g)2．2．3 单因素试验2．2．3．1 酶的浓度对原花青素得率的影响准确称取桉树叶粉末5份各1.0g分别置于圆底烧瓶中，加入相同体积70％乙醇溶液，分别加入浓度0.5% 1.0% 1.5% 2.0%的纤维素酶溶液各1.0mL，摇匀后移入60℃恒温水浴锅中，水浴50min后取出离心5min，滤液倒入量筒内，滤保山学院本科毕业论文（设计）渣再次60℃恒温回流90min，滤液倒入量筒内，取一定量两次上清液的混合液测定其吸光度值。
2．2．3．2酶解温度对原花青素得率的影响准确称取桉树叶粉末5份各1.0g分别置于圆底烧瓶中，加入相同体积70%乙醇溶液，分别加入浓度1.0％的纤维素酶溶液1.0mL，摇匀后分别移入40℃、50℃、60℃、70℃、80℃恒温水浴锅中，水浴50min后取出离心5min，滤液倒入量筒内，滤渣再次60℃恒温回流90min，滤液倒入量筒内，取一定量两次上清液的混合液测定其吸光度值。
2．2．3．3 酶解时间对原花青素得率的影响准确称取桉树叶粉末5份各1.0g分别置于圆底烧瓶中，加入相同体积70%乙醇溶液，分别加入浓度1.0％的纤维素酶溶液1.0mL，摇匀后移入60℃恒温水浴锅中，分别水浴30min、50min、70min、90min、110min后，取出离心5min，滤液倒入量筒内，滤渣再次60℃恒温回流90min，滤液倒入量筒内，取一定量两次上清液的混合液测定其吸光度值。
2．2．3. 4 料液比对原花青素得率的影响准确称取桉树叶粉末5份各1.0g分别置于圆底烧瓶中，各加入70%的乙醇溶液20mL、30 mL、40 mL、50 mL、60 mL，分别加入浓度1.0％的纤维素酶溶液1.0mL，摇匀后移入60℃恒温水浴锅中，水浴50min后取出离心5min，滤液倒入量筒内，滤渣再次60℃恒温回流90min，滤液倒入量筒内，取一定量两次上清液的混合液测定其吸光度值。
2．2．4正交试验设计在单因素试验基础上，对影响桉树叶原花青素提取效果的主要因素酶的浓度、酶解温度、酶解时间和料液比进行L16(45) 试验，因素水平见表1.桉树叶中原花青素的提取表1 正交试验因素水平设计因素水平料液比酶解温度酶解时间酶解浓度(A)／g ／mL (B)／℃ (C)／S (D)／％11:40 40 50 0.5 21:50 50 70 1.0 3 1:60 60 90 1.52.2.5原花青素含量的测定准确移取1.0ml 标准储备液于10mL 比色管中，再加入6．0mL 正丁醇－盐酸溶液( 95/5，V/V) 和0．2mL,2%硫酸铁铵溶液，旋紧试管于95℃±5℃的水浴中加热40min ，立即取出放入事先准备好的冷水中冷却15min 。