虾青素与Ⅱ型糖尿病研究进展

虾青素是1种海洋类胡萝卜素,它主要分布在海洋细菌,藻类,甲壳类和鱼类中。虾青素是自然界最强的抗氧化剂之一,有抗肿瘤发生、抗炎、抗糖尿病、抗肥胖等生物功能。目前国内外对虾青素在治疗糖尿病方面进行了大量研究,结果表明,虾青素对糖尿病及其并发症有预防和治疗作用。本文介绍了糖尿病的病因和发病机制,虾青素的生理功能,虾青素的概况,虾青素对Ⅱ型糖尿病的防治及相关作用机制的研究进展。     

红球藻提取物大鼠90d喂养试验与致畸试验研究

正天然虾青素在食品添加剂、保健品、制药业、化妆品等方面都有广泛的应用。国内外关于虾青素致畸试验的报道较少,有研究发现虾青素未引起胎兔畸形率的增加[1]。红球藻富含虾青素,是商业虾青素产品的良好来源。但关于红球藻提取物尚缺乏系统的毒理学     

虾青素纳米制剂研究进展及其策略分析

虾青素作为一种脂溶性的类胡萝卜素，具有强大的抗氧化性能，但因水溶性差，对温度、光、氧等外界环境敏感，生物利用度低等问题而限制了应用。新型纳米给药系统对于改善上述缺陷具有优势。该文就目前基于脂质、多糖和蛋白的虾青素新型纳米递送系统的研究现状和应用进行综述，并归纳与思考了虾青素纳米递送系统的研究方向，期望为虾青素的临床应用提供帮助。     

高效液相色谱法分析鉴定虾青素全反式、9-顺式、13-顺式几何异构体

目的 建立虾青素全反式、9-顺式和13-顺式异构体的高效液相色谱（HPLC）分析鉴定方法,优化一种碘诱导全反式虾青素异构化的方法。方法 采用高效液相色谱法,色谱柱为Shim-pack GIST C-18(1504.6 mm,5 μm),流动相为甲醇-乙腈-二氯甲烷-水（85:5.5:5:4.5）,检测波长为480 nm,流速为0.5 mL/min,进样量10 μL。为探究虾青素异构化条件,改良了一种碘诱导全反式虾青素异构化的方法,在曝光20 min后,分别对含碘量为5%~50%的10个虾青素样品溶液进行HPLC分析。结果 虾青素全反式、9-顺式和13-顺式异构体在该色谱条件下获得良好分离,经实验所得虾青素顺反异构体出峰顺序为全反式、9-顺式、13-顺式。异构化实验结果表明含碘量为15%的虾青素溶液经曝光后全反式、9-顺式、13-顺式异构体含量分别为对照品的68.5%、2436.7%和632.4%,为本实验的最佳比例。结论 本法准确、可靠,并较为便捷,在虾青素及其顺反异构体定量分析方面提供一定数据支撑,为虾青素制品在食品和医药方向的发展提供了理论依据。     

天然虾青紫的超级抗氧化活性及其应用

本文综述了天然虾青素的来源、超级抗氧化活性和生物安全性,以及在医药、保健食品和饲料工业中的应用,并对国内虾青素的产业化前景进行了展望。     

光照、加热对虾青素稳定性和抗氧化性的影响

目的考察光照、加热情况下虾青素的稳定性和抗氧化性的变化。方法配制一定浓度的虾青素溶液,分别经过阳光直射、紫外和加热处理,测定溶液中各虾青素异构体的浓度,并做1,1-二苯基-2-三硝基苯肼(DPPH)抗氧化性试验。结果在光照和加热条件下,减少的全反式虾青素转化为其顺式异构体,且主要转化为13-顺式异构体,对应的转化率分别为50%、100%。通过紫外照射试验发现,虾青素各异构体含量变化与光照相近,说明光照对虾青素的影响主要是由于其中的紫外光引起的。1,1-二苯基-2-三硝基苯肼清除试验表明,虾青素不止一种异构体有活性,且13-顺式异构体抗氧化性高于全反式。结论在光照和加热情况下虾青素容易发生降解以及异构体之间的转化。     

大规模培养雨生红球藻生产天然虾青素的研究进展和产业化现状

本文综述了近10年来国际上在雨生红球藻的生物学特性,细胞内积累天然虾青素的诱导条件方面的研究进展,以及应用光生物反应器大规模培养雨生红球藻工业化生产天然虾青素的现状,并对国内虾青素的产业化前景进行了展望。     

天然虾青素的提取、纯化研究进展

近年来虾青素的提取、纯化工艺在不断优化。微波、超声、超临界流体萃取术、生物酶法等技术可显著增加提取量。柱层析法、高效液相色谱法是最常见的纯化手段。该文综述了虾青素的提取、纯化研究进展,以期为提取、纯化方法的联合利用提供参考,促进虾青素的高效获取。     

虾青素药理作用的研究进展

虾青素是一种天然的类胡萝卜素,国外对其抗氧化、抗高血压、抗炎症、抗癌、抗辐射和增强免疫等药理作用进行了广泛研究。本文对近年来虾青素在药理作用方面的研究进展进行综述。     

虾青素生理活性的研究进展

虾青素是一种天然的萜烯类不饱和化合物,具有许多种对人类健康有益的生理活性。虾青素分子结构中有两个β-紫罗酮环和11个共轭双键,具有极强的抗氧化性和良好的生理活性,能够有效淬灭单线态氧、清除氧自由基、防紫外线辐射等,因而在食品、药品、化妆品等行业都有重要的应用。本论文介绍了虾青素的主要来源和结构特征,并对虾青素的一系列生理活性及其作用机制进行了综述,详细整理汇总了近年来虾青素在抗氧化、抗肿瘤、防癌症、光保护、视力保护、中枢神经的保护、抗炎症、预防心血管疾病等多方面新的研究成果,为虾青素未来的研究开发和综合利用提供依据。     

Ulcer preventive and antioxidative properties of astaxanthin from Haematococcus pluvialis

The anti-ulcer properties of astaxanthin fractions such as total carotenoid and astaxanthin esters from Haematococcus pluvialis were evaluated in ethanol-induced gastric ulcers in rats. Since oxygen radical release is a pathogenic factor of ethanol-induced gastric damage, astaxanthin - a free radical scavenger, was investigated as a potential ulcer preventive agent. Astaxanthin fractions - total carotenoid and astaxanthin esters were orally administered to experimental rats at 100, 250 and 500 microg/kg b.w. prior to ulcer induction. Alcian blue binding assay indicates that, total carotenoid and astaxanthin esters at 500 microg/kg b.w could protect gastric mucin approximately 40% and 67% respectively. Pre-treatment with astaxanthin esters, also resulted in significant increase in antioxidant enzyme levels - catalase, superoxide dismutase, and glutathione peroxidase in stomach homogenate. Histopathological examination substantiated the protective effect of astaxanthin in pre-treated rats. The increased antioxidant potencies such as free radical scavenging activity with an IC(50) of approximately 8 microg/ml and reducing power abilities (59 x 10(3) U/g) in vitro, reveal that H. pluvialis astaxanthin may protect gastric mucosal injury by antioxidative mechanism. In addition, approximately 23 fold increased lipoxygenase-inhibitory property, in comparison with standard astaxanthin and significant H(+), K(+)-ATPase-inhibitory activity of astaxanthin esters, in comparison with known proton pump blocking anti-ulcer drug - omeprazole, may envisage the potential gastroprotective effect by regulating the gastric mucosal injury and gastric acid secretion by the gastric cell during ulcer disease.     

In vivo protective efficacy of astaxanthin against ionizing radiation-induced DNA damage

Astaxanthin, a carotenoid pigment, is believed to be effective in the repair of DNA damage. Our study evaluates the effect of astaxanthin on DNA damage in rats exposed to whole-body radiotherapy using the comet assay. Thirty-two male rats were randomly divided into four groups (control, ionizing radiation, astaxanthin, and radiation+astaxanthin). The radiation and radiation+astaxanthin groups were exposed to X-rays at a dose of 8 gray (0.62 gray/min). Astaxanthin was administered at 4 mg/kg by gavage for 7 days starting from irradiation. The %TailDNA parameter was chosen as an indicator of DNA damage and the results were compared using one-way ANOVA. %TailDNA was 3.24 ± 3.12 in the control group, 2.85 ± 2.73 in the astaxanthin group, 4.11 ± 7.90 in the radiation group, and 3.59 ± 4.05 in the radiation+astaxanthin group. There was a significant increase in DNA damage in the radiation group, compared with the control and astaxanthin groups (p < .001). DNA damage was reduced in the radiation+astaxanthin group compared with the radiation group (p < .05). Although this decrease did not reduce damage to the level of the control group, it was significant. The decrease in radiation-induced DNA damage by astaxanthin administration in our study supports the hypothesis that astaxanthin is a promising agent for against/reducing DNA damage.     

Hypoglycemic effect of astaxanthin from shrimp waste in alloxan-induced diabetic mice

Hypoglycemic effect of astaxanthin obtained from shrimp waste was assessed in alloxan-induced diabetic and normal mice. Animals received oral administration of astaxanthin in dose of 5 and 10?mg/kg. The plasma glucose levels were examined and compared with that of metformin and gliclazide. Administration of astaxanthin (5 and 10?mg/kg) produced significantly fall on plasma glucose in alloxan-induced diabetic mice, while a slight fall in normal mice. In normal mice, postprandial hyperglycemia was significantly suppressed by oral administration of astaxanthin, which significantly lowered the postprandial area under curve. These results demonstrate that astaxanthin is effective in controlling hypoglycemia in animal model of type 1 diabetes mellitus. Therefore, astaxanthin can be a useful natural oral agent to treat diabetes.     

Effects of astaxanthin supplementation on exercise-induced fatigue in mice

The present study was designed to determine the effect of astaxanthin on endurance capacity in male mice aged 4 weeks. Mice were given orally either vehicle or astaxanthin (1.2, 6, or 30 mg/kg body weight) by stomach intubation for 5 weeks. The astaxanthin group showed a significant increase in swimming time to exhaustion as compared to the control group. Blood lactate concentration in the astaxanthin groups was significantly lower than in the control group. In the control group, plasma non-esterfied fatty acid (NEFA) and plasma glucose were decreased by swimming exercise, but in the astaxanthin group, NEFA and plasma glucose were significantly higher than in the control group. Astaxanthin treatment also significantly decreased fat accumulation. These results suggest that improvement in swimming endurance by the administration of astaxanthin is caused by an increase in utilization of fatty acids as an energy source.     

Safety assessment of astaxanthin derived from engineered Escherichia coli K-12 using a 13-week repeated dose oral toxicity study and a prenatal developmental toxicity study in rats

Astaxanthin is a natural carotenoid with strong antioxidant activity that has been used for decades as a nutrient/color additive and it has recently been marketed as a health supplement. Astaxanthin can be synthesized in a wide range of microalgae, yeast, and bacteria. As genes directing astaxanthin biosynthesis in various organisms have been cloned, this study assessed the safety of astaxanthin crystal produced by Escherichia coli K-12 harboring plasmids carrying astaxanthin biosynthetic genes. The astaxanthin crystal contains a total carotenoid content of 950 mg/g and an astaxanthin content of 795 mg/g. Subchronic oral toxicity and prenatal developmental toxicity of the astaxanthin in rats were conducted in accordance with the Guidelines of Health Food Safety Assessment promulgated by Food and Drug Administration of Taiwan which is based on OECD guidelines 408 and 414. Both male and female Sprague-Dawley (SD) rats (12 for each gender) receiving the astaxanthin crystal at 1.2, 240.0, or 750.0 mg/kg/day in olive oil via oral gavage for 90 days showed no changes in body weight gains, hematology and serum chemistry values and hepatic enzyme stability, organ integrity and organ weight. Except the higher food consumption observed in rats receiving 750.0 mg/g astaxanthin crystal, administration of the astaxanthin crystal to 25–27 pregnant female rats in each group throughout the period of organogenesis (G6-G15) produced no adverse effects on fetal organogenesis. Based on the results, we propose that the no-observable-adverse-effect level (NOAEL) of the astaxanthin crystal extracted from genetically modified E. coli K-12 is 750.0 mg/kg bw/day.     

Characterization of metabolites of astaxanthin in primary cultures of rat hepatocytes.

The metabolism of the nonprovitamin A carotenoid astaxanthin was investigated in primary cultures of rat hepatocytes. In a time course study based on HPLC and gas chromatography-mass spectrometry analyses, one main metabolite, (rac)-3-hydroxy-4-oxo-beta-ionone, was found. This metabolite was conjugated mainly into glucuronides, as demonstrated by glusulase treatment of the conjugates under sulfatase-inhibiting conditions. Within 24 h more than 50% astaxanthin was metabolized and conjugated. Deconjugation of the polar conjugates with glusulase and analyses with HPLC and gas chromatography-mass spectrometry identified two metabolites, (rac)-3-hydroxy-4-oxo-beta-ionone and its reduced form (rac)-3-hydroxy-4-oxo-7,8-dihydro-beta-ionone, indicating that the former was reduced in the conjugated form. We confirmed that the ketocarotenoid astaxanthin induces xenobiotic-metabolizing enzymes in rat liver in vivo. However, there were no differences in the metabolism of astaxanthin in cultured hepatocytes from rats that were pretreated with astaxanthin and, thus, with induced cytochrome P-450 systems compared with control hepatocytes. Neither liver microsomes from astaxanthin-pretreated nor control rats metabolized astaxanthin. These results indicated that the cytochrome P-450 enzymes were not involved in the metabolism of astaxanthin in rat hepatocytes. We conclude that astaxanthin was metabolized in primary cultures of rat hepatocytes into (rac)-3-hydroxy-4-oxo-beta-ionone and its reduced form (rac)-3-hydroxy-4-oxo-7,8-dihydro-beta-ionone independent of the xenobiotic-metabolizing enzymes induced by astaxanthin.     

Dissolution and spectrophotometric determination of astaxanthin in aqueous solutions

The poor solubility of astaxanthin in water can cause problems during dissolution tests of dosage forms because they are usually performed in water-based media. The aim of this study was the development of a convenient dissolution medium and a method for a spectrophotometric determination of astaxanthin in an aqueous solution. Three surfactants in different concentrations were tested as solubility-improving substances: sodium lauryl sulfate (SLS), polysorbate 80 (PS 80) and macrogolglycerol hydroxystearate (Cremophor RH 40, CR 40). Optimal conditions were determined. The dissolution of astaxanthin from solid dosage form is performed into 1000 g of a solution of sodium lauryl sulfate with the concentration 1.0% (w/w) at 37 degrees C by paddle method, 100 rotations per minute, dissolution time 30 minutes. The procedure is convenient for solid dosage forms with a content of 4 to 12 mg of astaxanthin. The spectrophotometric determination of astaxanthin in aqueous solution from the dissolution test is measured at 486 nm. The specific absorbance A(1%) 1cm for astaxanthin in water is 2000, a sodium lauryl sulfate solution (1%) was used as a blank.     

Protective effect of astaxanthin on naproxen-induced gastric antral ulceration in rats

Frequently used for humans as non-steroidal anti-inflammatory drug, naproxen has been known to induce ulcerative gastric lesion. The present study investigated the in vivo protective effect of astaxanthin isolated from Xanthophyllomyces dendrorhous against naproxen-induced gastric antral ulceration in rats. The oral administration of astaxanthin (1, 5, and 25 mg/kg of body weight) showed a significant protection against naproxen (80 mg/kg of body weight)-induced gastric antral ulcer and inhibited elevation of the lipid peroxide level in gastric mucosa. In addition, pretreatment of astaxanthin resulted in a significant increase in the activities of radical scavenging enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. A histologic examination clearly proved that the acute gastric mucosal lesion induced by naproxen nearly disappeared after the pretreatment of astaxanthin. These results suggest that astaxanthin removes the lipid peroxides and free radicals induced by naproxen, and it may offer potential remedy of gastric ulceration.     

虾青素可能通过H~+传递功能保护NaN_3损伤的人胎肝L-02细胞

观察虾青素(astaxanthin)对呼吸链复合体Ⅳ抑制剂叠氮钠(NaN3)损伤的人胎肝L-02细胞保护作用,并初步探讨其作用机制。100 mmol·L-1 NaN3用于构建肝损伤细胞模型,通过测定不同浓度虾青素(0.01、0.10、1.00及10.00 nmol·L-1)对损伤细胞存活率(MTT检测)、细胞内活性氧(reactive oxygen species,ROS)水平(DCFH-DA检测)、细胞凋亡率(Annexin V-FITC/PI双染法)以及线粒体膜电位(mitochondrial membrane potential,MMP)水平(JC-1法)的影响,发现虾青素能抑制损伤细胞晚期凋亡;对细胞存活率和MMP的保护作用呈现先增加后降低的非剂量依赖性关系,其中0.10 nmol·L-1虾青素表现为较强的保护作用;实验浓度范围内的虾青素并不能显著降低细胞内ROS水平(P>0.05)。为进一步探讨虾青素对损伤细胞的保护作用,人工制备平面双层磷脂膜(planar bilayer lipid membrane,BLM)模拟线粒体膜,测定不同浓度虾青素(0.1%、2.0%、10.0%)对H+的传递能力。结果...