红花 (Carthamus tinctorius)


别名/常用名称/相关术语

18:2,美国红花,菊科(家族),混种红花,Carthamus tinctoriusCarthamus tinctorius L.,菊科(家族),代尔红花,EH0202,假红花,假红花,高油酸红花油,hing hua,honghua ,Intralipid® , kinobeon A,亚油酸,亚油酸,Liposyn® ,Liposyn® II,改良Liposyn® , Microlipid® ,单不饱和脂肪酸,MUFA,n-6,n-6多不饱和脂肪酸,富含n-6植物油,非酯化脂肪酸(NEFA),notoginseny cream,N-(对香豆酰)5-羟色胺,油酸酯,omega 6,多不饱和脂肪,多不饱和脂肪酸,PSF,PUFA,SAF,红花注射液,红花粉,红花油,红花油饼,红花油乳剂,红花油酯,红花油基脂肪乳剂(TPN + L组),红花瓣,红花籽,红花黄,红花油,Safola® ,生育酚,甘油三酯,US,花绀青,查菲兰

 

红花中的生物活性物质

 

作用机理
 
药理学:
  • 成分:红花(Carthamus tinctorius, L.)中含有红花黄、chalconoid化合物、羟基红花黄色素A64和色素kinobeon A。
  • 红花籽中含有N-(对香豆酰)5-羟色胺65,66
  •  红花油的成分包括6%棕榈酸,12%油酸18,74%亚油酸18和omega-6亚油酸,具有两个双键67。红花油饼的衍生物包括:N-[2-(5-羟基-1H-吲哚-3-基)乙基]草酰胺、N-[2-(5-羟基-1H-吲哚-3-基)乙基] -对香豆酰胺、N,N'-[2,2'-(5,5'-二羟基-4,4'-联-1H-吲哚-3,3'-基)二乙基]-二-对香豆酰胺、N-[2-[3'-[2-(对香豆酰胺基)乙基]-5,5'-二羟基-4,4'-联-1H-吲哚-3-基]乙基]阿魏酰胺和N,N'-[2,2'-(5,5'-二羟基-4,4'-联-1H-吲哚-3,3'-基)二乙基]二茶酰胺、N-[2-[5-(β-D-葡糖氧基)吲哚-3-基)乙基]-对-香豆酰胺和N-[2-[5-(β-D-葡糖氧基)-1H-吲哚-3-基)乙基]草酰胺。68
  • 抗癌效果:一项回顾性病例-对照研究数据表明籽油的摄入与乳腺癌风险之间的反相关关系,包括红花油。69
  • 在一项体外研究中,含有人参和红花的草药提取物中的化合物(珠香)在MDA-MB-231乳腺癌细胞和正常人类乳腺细胞系中显示出对细胞增殖显著的剂量依赖性抑制,并比常用的细胞毒性药物具有更大的抑制作用。2
  • 根据一项动物研究,富含n-6多不饱和脂肪酸(红花油)的高脂肪饮食的效果取决于油的摄入时间:如果在肿瘤细胞接种之前,这种饮食促进肿瘤生长,而如果在肿瘤增殖开始之后就没有影响。31这表明n-6多不饱和脂肪酸可促进结肠癌增殖的开始,但一旦形成之后就不会对肠癌的增殖起促进作用。
  • 在一项体外研究中,红花油可对HT-29恶性人肠癌细胞系起抑制作用。70而在另一项体外研究中,含有大量甘油三酯亚油酸酯的红花油相对于正常黑素细胞会选择性更多的抑制恶性黑素瘤的生长。71
  • 抗炎症效果:根据一项体外研究,红花籽中的N-(对香豆酰)5-羟色胺及其衍生物对可单核细胞的促炎细胞因子起抑制作用。65,66其他的体外研究表明N-(对香豆酰)5-羟色胺及其衍生物可通过多种机制抑制促炎细胞因子的产生。66此外,5-羟色胺衍生物N-(对香豆酰基)5-羟色胺与碱性成纤维细胞生长因子(bFGF)或表皮生长因子(EGF)协同增强正常人和小鼠成纤维细胞的增殖。此外,各种体外和动物研究表明,红花黄可使非特异性和特异性免疫功能下降。64红花油对血脂异常患者的膳食补充并不会显著影响C反应蛋白、血清淀粉样蛋白A和IL-6浓度,但可降低胆固醇的水平。73
  • 抗氧化效果:从红花(Carthamus tinctorius L.)油饼中分离出七种抗氧化血清素衍生物。68他们的结构经确定为:
  • N-[2-(5-羟基-1H-吲哚-3-基)乙基]草酰胺
  • N-[2-(5-羟基-1H-吲哚-3-基)乙基]-对香豆酰胺
  • N,N'-[2,2'-(5,5'-二羟基-4,4'-双-1H-吲哚-3,3'-基)二乙基]-二-对香豆酰胺
  • N-[2-[3'-[2-(对香豆酰胺基)乙基]-5,5'-二羟基-4,4'-双-1H-吲哚-3-基]乙基]阿魏酰胺和N,N'-[2,2'-(5,5'-二羟基-4,4'-联-1H-吲哚-3,3'-基)二乙基]-二叶草酰胺,N-[2-[5-(β- D-葡糖基氧基)-1H-吲哚-3-基)乙基]对香豆酰胺和N-[2-[5-(β-D-葡糖氧基)-1H-吲哚-3-基)乙基]草酰胺。
  • 通过硫氰酸铁法和α,α-二苯基-β-苦基肼基(DPPH)法测量化合物的抗氧化活性,并且仅有N-[2- [5-(β-D-葡糖氧基)-1H-吲哚-3-基]乙基]-对-香豆酰胺和N-[2-[5-(β-D-葡糖氧基)-1H-吲哚-3-基)乙基]阿魏酰胺被发现没有较强的抗氧化活性。
  • 在一项临床试验中,补充红花油减少了膜磷脂总n-6和总n-3脂肪酸与年龄相关的差异。74 在摄入红花油的人类血液样本中,16:0,18:0,18:1n-9和22:5n-6仅增加在年轻的鬼影细胞中,并且红花油的摄入增加了年轻和衰老红细胞对由自由基导致氧化损伤的敏感性(p <0.001)。75
  • 根据一项动物实验,补充n-3脂肪酸不会影响循环红细胞中的脂质过氧化和蛋白质聚集,但在有氧条件下确实会增加过氧化作用,但不会增加分离红细胞中的蛋白质聚集。76在一项实验室的研究中,总自由基由于酚类化合物的存在,红花油可具有显著的清除能力。77
  • 体脂组成效果:喂食具有单不饱和脂肪酸和多不饱和脂肪酸的高油酸或高亚油酸红花籽的羔羊组织增加了组织中18:1(反式-11)和共轭亚油酸(CLA),这对于当前人类饮食指南将会带来有利的改变。78
  • 血压效果:在一项临床研究中,血压正常的成年人摄入红花油并未显示收缩压或舒张压的任何显着变化,但静息平均动脉压显着下降至79 +/- 2(p <0.05)。20
  • 在一项临床试验中,全血和血浆粘度以及红细胞Li/Na反向转运,Na/K共转运和Na泵系统(V max)均未因亚油酸的摄入而改变。24
  • 在一项临床研究中,在8名患有原发性高血压的白人男性中,50毫升红花油(39克n-6脂肪酸)并未对血压产生显著影响。38
  • 致癌效果:在大鼠中,富含n-6多不饱和脂肪酸的饮食促进了肿瘤前损伤和肿瘤的发展。26含有红花油的高脂饮食也显示出对肝脏IGFBP-1惊人的诱导作用,这种蛋白已被证明与肝癌发展具有关联。
  • 动物研究表明,在玉米和红花油中发现的n-6类的膳食多不饱和脂肪酸(PUFA)可能是涉及乳腺肿瘤发展的中间体的前体,而在鱼油中发现的长链(LC)n-3 PUFA可能会抑制这些作用。28,29 根据一项临床试验的结果,总n-6 PUFA在美国可能导乳了腺癌的高风险,而来自于鱼油中的LC n-3 PUFA则可能具有保护的作用。28 在另一项动物研究中,在5%玉米油和2%亚油酸饮食组中观察到最常见的微转移,但这些差异并不具有统计学上的显著性。30
  • 根据一项动物研究,富含n-6多不饱和脂肪酸(红花油)的高脂肪饮食的效果取决于油的摄入时间:如果在肿瘤细胞接种之前,这种饮食促进肿瘤生长,而如果在肿瘤增殖开始之后就没有影响。31 这表明n-6多不饱和脂肪酸可促进结肠癌增殖的开始,但一旦形成之后就不会对肠癌的增殖起促进作用。
  • 心血管作用:在针对进行过体外循环手术后成人患者的一项临床试验中,30分钟的Liposyn®  10%和Intralipid®  10%静脉注射对左心室卒中、左心室充盈压、心输出量、全身血管阻力、平均系统动脉血压、中心静脉压或平均肺动脉压并未引起显著的变化。4
  • 细胞效果:在一项针对正常血压志愿者的临床试验中,每天摄入4g红花油,与安慰剂治疗相比,可显着降低积极治疗结束时的白细胞电离钙水平。22作者得出结论:细胞膜脂肪酸在白细胞中可调节细胞内的钙离子,因而可能在其他组织中也是如此。这些作者的早期临床试验中也观察到了类似的结果。23
  • 根据临床试验,在生理浓度下,膜亚油酸含量影响跨膜钠通量,但不通过调节钠泵活性。79
  • 凝血效果:在一项临床试验中,不同浓度的α-亚麻酸日常饮食并不影响素食男性的血栓形成风险因素。37另一项临床试验显示,10%红花油乳剂(Liposyn® 10%)的输注降低了Lee-White凝血的时间。9在体内进行亚油酸日常饮食对人体血小板功能影响的检测显示48小时内血小板聚集时间显着增加,这是增加的4%卡路里的亚油酸膳食而引起的变化,而相应的解聚时间在96小时内显著下降。只有0.5%的卡路里变化与4天内的显著变化相关。
  • 根据临床试验,每天摄入60mL红花油将血小板亚油酸(C18:2 omega 6)含量从5.53 +/-0.52 μg增加至10.1 +/-0.92 μg/100 μg总脂肪酸(p <0.001),并将血小板的聚集减少至ADP;纤维蛋白溶解和出血的时间不变。10
  • 根据一项关于鱼油对高血压影响的随机研究,在8名患有原发性高血压的白人男性中,50毫升红花油(39克n-6脂肪酸)并未显着改变血清血栓素的水平。38
  • 认知/记忆效果:在摄入15分钟后,红花油的能量摄入便可改善延迟段回忆(p <0.001),并对即时段回忆(p <0.04)也有改善,而这与血糖的升高无关。80此外,脂肪引起的改善通过在60分钟后(p <0.05)。
  • 皮肤病学效果:在实验室研究中,由红花细胞培养物产生的kinobeon A表现出对人酪氨酸酶活性的强烈抑制。34
  • 内分泌效果:带有红花油(18:2)的高脂喂养大鼠产生了胰岛素抵抗并因通过特异性增加的18:2-CoA增加了总长链酰基-CoA(LCACoA)含量(p <0.0001)。8然而,临床研究中,接受4g红花油安慰剂膳食了8周的年轻久坐的个体(年龄21.5±0.4岁(平均值±SEM);体重,77.6±3.4kg)并未发现胰岛素敏感性指数的变化55
  • 在一项临床试验中,与基线相比,红花油的补充使得空腹血糖升高了11%(p <0.05),而体重、空腹血清胰岛素水平和胰岛素敏感性并没有变化。空7腹血糖的绝对增加值与基线空腹血糖(红花油,r = 0.75,p = 0.012)相关。
  • 肝脏效果:在一项动物研究中,喂食含10%红花油的大鼠肝脏中Delta-5和Delta-6去饱和酶的mRNA水平只有无脂饮食或含有三油酸甘油酯饮食的大鼠肝脏中的25%。32在另一项大鼠研究中,含有红花油的高脂饮食显示出对肝脏IGFBP-1的惊人诱导,而该蛋白已被发现与肝癌发展相关。26
  • In a clinical trial in four undernourished adults (15%-37% below ideal body weight) on fat-free total parenteral nutrition, supplementation with oral linoleic acid (as safflower oil) reversed the elevation of serum liver enzymes.81
  • 在四个营养不良成年人(低于理想体重15%-37%)对无脂全肠外营养的临床试验中,口服补充亚油酸(如红花油)可逆转血清肝酶的升高。81
  • 高血脂症效果:红花油的替代物可导致胆固醇亚油酸酯的增加,而胆固醇亚油酸酯是主要的胆固醇酯脂肪酸之一。45根据一项临床试验的结果,每天摄入60mL红花油可降低血清胆固醇。10含有亚油酸的n-6富含植物油如红花油的高血脂症作用仍然不清楚。82,83临床数据表明,与富含黄油的膳食相比,富含椰子油和红花油的膳食中的胆固醇合成较低,并且可能与含有载脂蛋白B的脂蛋白的低产率有关。39胆固醇的积聚可能是由于增强的胆固醇酯转移与载脂蛋白B脂蛋白结合以及肝脏对胆固醇的摄取增加,可能有助于高油酸红花油(单不饱和脂肪酸,MUFA)和红花油(多不饱和脂肪酸,PUFA)在胆固醇酯转移蛋白转基因小鼠(CETP)中的降胆固醇作用。40在一些高脂血症人群中进行的临床试验中,红花油被用作安慰剂,并没有显著改变任何脂质/脂蛋白值。48,49,50,51,52,53根据一项临床试验的结果,与黄油相比,红花油对血浆胆固醇浓度没有明显影响,但与三酰甘油缓慢升高有关。32临床证据显示,油酸在降低正甘油三酯血症患者中的低密度脂蛋白胆固醇水平时与亚油酸一样有效,并且油酸似乎比亚油酸降低HDL-C水平的频率更低。44两种不饱和脂肪对高甘油三酯血症患者的脂蛋白水平均有显著影响。另外,静脉内脂肪乳剂中亚油酸和α-亚麻酸的含量导致接受全胃肠外营养的婴儿的总血浆脂质的脂肪酸谱的统计学显著变化。84用α-亚麻酸替代亚油酸不会改变血脂正常的男性的血脂。54在另一项临床试验中,红花油添加到极低脂肪(VLF)素食中导致18:2和20:4 omega 6的显著增加,以及18:1、20:5 omega 3和22:5 omega 3的显著降低。46这些结果表明,通过降低饮食中的总脂肪含量或通过用不饱和脂肪交换饱和脂肪来降低饮食中饱和脂肪含量(<6%饮食能量),总血浆胆固醇水平在正常胆固醇胆固醇受试者中可降低约12%。在Schnell等人的临床试验中,主要脂肪来源为红花油的多不饱和脂肪饮食使平均HDL(2)滞后时间从45.8 +/- 12.5增加到83.3 +/- 11.6分钟,而氧化速率并没有变化。85维生素E的添加进一步将HDL(2)滞后时间增加至115.6±4.4分钟并且将HDL(2)氧化速率降低10倍。 因此,在控制膳食脂肪摄入的条件下,高多不饱和脂肪摄入量不会增加HDL亚组分的氧化敏感性,并且在此情况下,维生素E补充会降低HDL的氧化易感性(2)。 在一项临床研究中,LDL中的载脂蛋白B因聚烯磷脂酰胆碱和苯胺油而显著降低。41两种物质的作用在降低载脂蛋白B和可能的胆固醇方面具有可比性。 根据对16名健康男性进行的一项随机双盲试验,摄入红花油来源的38-40%能量可降低血清总胆固醇15%(p <0.001),LDL-胆固醇20%(p <0.001),和apo B-100 21%(p <0.001)。42总体而言,88%(N = 14)的受试者血清总胆固醇水平从基础饮食值下降> 10%。
  • 在针对肥胖受试者的一项临床试验中,补充玉米和红花油的两周和四周液体饮食处理可将二高-γ-亚麻酸(C20:3n-6)浓度降低44%并将花生四烯酸(C20:4n-6)增加26%,但血清磷脂亚油酸(C18:2n-6)的浓度则保持恒定。6
  • 在一项血管疾病患者的临床试验中,富含多不饱和脂肪酸的膳食可导致丙二醛修饰的低密度胆固醇(MDA-LDL)的抗体减少。43这种下降与基线相比在1小时(p <0.05)、两小时(p <0.004)和三小时(p <0.02)均具有统计学意义,而最低点在两小时。
  • 免疫效果:富含n-6多不饱和脂肪酸(n-6 PUFA)的红花油可影响败血症动物的存活率并降低免疫功能。13在一项针对维持红花油乳剂肠外营养的婴儿的临床试验中,灌注红花油乳剂不会细胞免疫功能产生不利的影响。56在一项动物研究中,在小鼠出血模型中摄入红花油相对于对照组可导致腹膜巨噬细胞释放PGE2的显着增加、腹膜巨噬细胞抗原呈递能力的显着抑制、白细胞介素1的释放、脾细胞增殖和白细胞介素2的分泌。14在体外研究中,红花油作为多元不饱和脂肪酸控制的异亚麻酸没有使得细胞因子的分泌发生改变。57在一项动物研究中,红花多糖通过Toll样受体4激活了转录因子NF-κB,并通过巨噬细胞诱导了细胞因子的产生。15在一项临床试验中,补充了红花油的低脂肪饮食可增加自然杀伤细胞活性,相应的E/T比率为100:1(每份脂肪卡路里的绝对百分比增加约0.79%,p =0.04)。16在一项临床试验中,口服富含亚油酸的红花油(母体n-6脂肪酸)在24小时期间不会影响淋巴细胞的增殖。58
  • 一项随机的前瞻性双盲研究对艾滋病毒携带者的鱼油免疫调节作用进行了分析,以红花油用作对照并没有显示出明显的活性。59
  • 在一项前瞻性临床研究中,为烧伤患者采用新的膳食(乳清蛋白提供能量的20%,精氨酸提供2%,半胱氨酸提供0.5%和组氨酸提供0.5%;非蛋白脂质提供的15%中鱼油和红花油各占一半)与其他标准肠内制剂相比可减少伤口的感染(p <0.03),缩短住院时间(p <0.02)并且减少死亡(p <0.06)。17
  • 炎症效果:根据一项关于鱼油对高血压影响的随机研究,在8名患有原发性高血压的白人男性中,50mL红花油(39克n-6脂肪酸)并未显着增加前列腺素(PG)E2的形成。38在一项动物研究中,在小鼠出血模型中摄入红花油相对于对照组可导致腹膜巨噬细胞释放PGE2的显着增加、腹膜巨噬细胞抗原呈递能力的显着抑制、白细胞介素1的释放、脾细胞增殖和白细胞介素2的分泌。14
  • 代谢效果:在一项动物研究中,将红花油灌注至大鼠的十二指肠并没有对代谢率产生影响。86
  • 在一项针对肥胖型非糖尿病受试者的临床试验中,红花油抑制了糖原分解的速率,但在脂质输注后又不受棕榈油的抑制,表明饱和脂肪酸和PUFA对肝糖代谢具有不同的作用。18血浆非酯化脂肪酸浓度的急剧变化不会改变2型糖尿病患者的肝脏葡萄糖生成。87
  • 根据一项临床试验的结果,口服脂肪(红花油)可因为人体内储存的脂质释放而增加第一阶段甘油三酯的浓度。62,63有人提出,因感官增强而引起的残留池中脂质的释放导致了三酰甘油酯早期的上升,这增加了因脂质膳食吸收而造成的峰值;这反过来又补充了与释放内源合成的甘油三酯相关的后期峰值,因为所有三种来源的脂质会竞争共同的清除机制。此外,单纯的脂肪的味觉也会升高餐后的三酰甘油水平。63其他的一些数据也表明,人类口鼻部位存在一种化学感觉或触觉机制,可用于检测膳食脂肪化学成分的某些方面,或是源自脂肪或携带脂肪的成分,从而引发餐后脂质代谢的变化。88
  • 诱变效果:通过使用鼠伤寒沙门氏菌TA97a,TA98,TA100以及TA102株的诱变研究表明红花并不具有碱基替换的诱变活性。27然而,一些动物研究的结果表明膳食中n-6 PUFA可强烈诱导肝脏中胰岛素类生长因子结合蛋白1(IGFBP-1)的表达,而该蛋白与肝癌的发展具有关联。26
  • 血小板聚集效果:在一项体内研究中,因为膳食亚油酸的含量增加了4%,48小时内血小板聚集时间显着增加,而解聚时间在96小时内显着下降。11在另一项临床试验中,不饱和脂肪酸(红花油)的摄入减少了因三周高油饮食喂养而导致的血小板聚集(p <0.01)。12另一项临床试验的结果表明红花在阻止血小板聚集、抗凝和促进微循环方面发挥了作用。1
  • 前列腺素(PG)效果:在一项临床试验中,8小时的Liposyn® 10%灌注可显着增加可被免疫测定的6-oxo-PGF1α的分泌。89而同时可被免疫测定的PGE分泌则缓慢增加。在另一项儿科的临床研究中,20%的红花油乳剂被发现可在短时间内增加了脂肪组织中亚油酸和花生四烯酸的浓度。65根据临床研究,50mL的红花油(39克n-6脂肪酸)并不显著增加原发性高血压患者前列腺素E2的形成。38在一项动物研究中,在小鼠出血模型中摄入红花油相对于对照组可导致腹膜巨噬细胞释放PGE2的显着增加、腹膜巨噬细胞抗原呈递能力的显着抑制、白细胞介素1的释放、脾细胞增殖和白细胞介素2的分泌。14
  • 呼吸效果:在一项动物研究中,母亲喂养了高n-6多不饱和脂肪酸(PUFA)(红花油)的新生大鼠表现出肺脂质中n-6多不饱和脂肪酸的增加和对高氧暴露的超强耐受性。90与正常饮食后代相比,高n-6和高n-3饮食标准的后代表现出基本上相同强高氧耐受性[7天(>95% O 2 )分别110/115和99/109 vs. 70/91的生存率, p<0.01]。
  • 饱腹感效果:根据一项临床试验的结果,以油或全食物形式提供的膳食脂肪引起的饱腹感反应受性别影响,并且取决于脂肪对于女性而非男性中胆囊收缩素释放的刺激。91
  • 血清脂质效果:在一项临床试验中,红花油消耗量不会增加血浆共轭亚油酸浓度。61在一项I期的临床试验中,摄入红花油可显著升高亚油酸的高磷脂和甘油三酯组分,并显著升高花生四烯酸的磷脂组分;油酸的磷脂组分显着下降,而棕榈酸的甘油三酯组分也显着下降。92
  • 在两项临床研究中,红花油的摄入并未减弱n-3 PUFA(鱼油)对心血管疾病的某些危险因素(膜脂肪酸组成,血脂和血栓形成特征)的有利调整。60
  • 根据临床研究,在8名患有原发性高血压的白人男性中,50mL红花油(39克n-6脂肪酸)略微增加了磷脂中的亚油酸。38
  • 在一项临床试验中,红花油的摄入不会像橄榄油一样增加餐后乳糜微粒的残留量。19
  • 根据一项针对新生儿使用α-亚麻酸作为0.1%或3.0 +/- 1.5%(SD)的脂肪酸全肠外营养的临床试验中,α-亚麻酸和二十碳五烯酸在高α-亚麻酸组中提到了升高;然而,在两个研究组中静脉内脂肪治疗期间亚麻酸的另一代谢物二十二碳六烯酸发生了下降。25两个研究组均显著降低了花生四烯酸水平并且使亚油酸和花生四烯酸的比例增加。
  • 根据一项临床研究,由于与EFAD相关的红细胞更新率增加,患有必需脂肪酸缺乏症(EFAD)的患者在红细胞膜中掺入血浆脂肪酸的发生率与没有EFAD的可能不同。93
  • 在四个营养不良成年人(低于理想体重的15%-37%)的无脂全肠外营养的临床试验中,口服补充亚油酸(如红花油)逆转了必需脂肪酸缺乏症。81
  • 在一项临床试验中,含有红花油膳食的研究者血浆中亚油酸的比例提到了提升。21
  • 在一项针对轻度至中度高胆固醇血症男性的临床试验中,血浆中的细胞胆固醇显著增加(11%,p <0.004)并高于禁食血浆的值,甘油三酯血症患者的细胞胆固醇含量也显著增加(70%,p <0.001)但在LDL级分中显著降低(p = 0.006),此外在餐后血浆中血浆胆固醇酯化存在较小的(5%)显著(p <0.001)增加。47
  • 在高甘油三酯血症、非胰岛素依赖型糖尿病受试者的临床试验中,从红花油饮食转向鱼油饮食显著降低了总血浆甘油三酯(p = 0.01)和VLDL-apoB(p = 0.04)的量,但并没有降低 LDL或总血浆apoB的量。94
  • 子宫刺激效果:根据一项实验室研究的结果,红花可对体外小鼠子宫具有刺激作用,而这可能与刺激子宫的H1受体和α-肾上腺素能受体有关。35

 

药效学/动力学:
  • 囊性纤维化患者的吸收:在小儿囊性纤维化受试者的临床试验中,在没有胰酶的情况下消耗的红花油(甘油三酯)在后续的四小时内并没有提高血浆亚油酸的平均水平。33当摄入亚油酸甘油酯(LAM)后,血浆亚油酸水平在两小时(p <0.02)、三小时(p <0.01)和四小时(p <0.01)时均显著高于红花油。当摄取游离脂肪酸(水解红花油)时,囊性纤维化及对照儿童中血浆亚油酸的水平几乎没有增加。当囊性纤维化儿童也服用胰酶时,从甘油三酯而非亚油酸单甘油酯中吸收的亚油酸将会更多。三个患有囊性纤维化的儿童在服用胰腺胶囊的同时加入抗酸剂和西咪替丁时,摄入红花油后血浆中亚油酸的水平比他们单纯服用胰腺胶囊时增加的更多。在一项95临床试验中,通过研究高红花油膳食之后的0、2、4、6和8小时获得的血浆样品表明,当以常规剂量的胰酶补充剂给药时,囊性纤维化患者可吸收所有的红花成分。许多可用作必需脂肪酸状态指标的参数计算结果表明囊性纤维化中存在必需脂肪酸的缺乏。用红花油(每日1g / kg)治疗11名囊性纤维化患者并未能纠正脂肪酸模式中的异常。96生化数据表明,亚油酸至花生四烯酸酯的转化和吸收过程可能受损。然而,单靠吸收不良不能解释囊性纤维化患者的不足或边缘性必需脂肪酸状况。97利用红花油进行的一项吸收研究证明了必需脂肪酸的正常肠内吸收和可穿过血脑屏障的能力。98在囊性纤维化患者中有限的亚油酸量导致了红细胞形状的变化,这可能是通过降低了膜中亚油酰磷脂酰胆碱含量的直接作用结果,也可能是通过影响酶活性的间接作用结果。99
  • 清除:在一项临床研究中,向健康志愿者施用以10%或20%红花油乳剂(Liposyn® ) 形式的0.1g脂肪/千克体重,结果表明两种乳剂之间的清除率并没有显著差异。3可得出的结论是, 20%脂肪乳剂用于静脉的营养支持和10%的脂肪乳剂是一样安全的。由Burckart等人进行的一项新生儿研究发现较小的新生儿可能存在相对较为缺陷的自由脂肪酸清除能力。5
  • 代谢:红花黄B可由人类的肠道细菌进行代谢。100
  • 根据临床试验的结果,来自血浆乳糜微粒,特别是亚油酸的膳食脂肪酸可迅速转移到人的乳液中。36在红花油摄入后10小时后可达到最大的增加并且在乳液中保持10-24小时的显著升高(p<0.05)。
  • 在对80名健康志愿者进行连续小剂量的肝素输注期间摄入至609 +/- 37μmol/L时,18:2 n-6脂肪酸的血浆浓度升高了两小时。101
  • theonin 54(T54)携带者的代谢:肥胖和T54携带者的餐后脂血对于乳糜微粒胆固醇和乳糜微粒三酰甘油曲线下的区域是显着的[较高的红花值 (分别为0.635 +/- 0.053和2.48 +/- 0.30mmol. 小时/L)相对于橄榄油(分别为0.592 +/- 0.052和2.48 +/- 0.32mmol. 小时/L)或(分别为0.425 +/- 0.043和1.69 +/- 0.20mmol. 小时/L); p<0.05]。102
  • 稳定性:调查了用于新生儿和婴儿患者的三种不同的一体化外加剂中1:1-大豆/红花静脉内脂质乳剂的稳定性。在所研究的三种一体化组合物之一中,大豆/红花的混合物稳定性显著并可实现迅速恶化。在另一项早期的研究中,也观察到了同样显著稳定性和迅速恶化。104

 

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