Fucoidan regulate blood glucose homeostasis in C57BL/KSJ m+/+db and C57BL/KSJ db/db mice

Type 2 diabetes mellitus is a multisystem disease that is characterized by hyperglycemia and is associated with the dysfunction and failure of various organs. The control of postprandial hyperglycemia is important in the prevention and intervention of type 2 diabetes. Fucoidan has several biological activities in vitro and in vivo. However, the effect of fucoidan on hyperglycemia in non-diabetic and diabetic mice has not been investigated. This study was undertaken to study the effects of different molecular weight forms (5 kilodalton (k), 5-30 k and crude) of fucoidan on oral glucose tolerance tests in non-diabetic mice and on food intake, weight gain, fasting blood glucose and blood biochemistry of db/db mice. Treatment with 200 mg/mL 5 k, 5-30 k and crude fucoidan substantially prevented hyperglycemia according to oral glucose tolerance tests in non-diabetic mice. In addition, fucoidan fractions significantly reduced blood glucose levels in diabetic mice.     

海带岩藻聚糖硫酸酯电渗析分离工艺

采用电渗析法对盐沉后的海带酶解液中岩藻聚糖硫酸酯进行分离,探索工业化分离生产岩藻聚糖硫酸酯的方法,以解决目前乙醇沉淀法存在的安全性和高成本等问题。以脱盐率、糖保留率为检测指标,采用响应面法优化了电渗析工艺参数。结果显示,在操作电压80 V、料液流量3.2 L/min、固形物浓度10 mg/ml、p H=5的条件下,电渗析连续循环3次,海带酶液解干基中多糖含量由40.17%提高至47.11%,硫酸根含量由3.36%提高至4.97%。电渗析后海带酶解液干基中的金属离子含量为Ca 0.13 mg/g、Mg 16.04μg/g、Cu 0.29μg/g、Se 11.7μg/g、Cr 8.06μg/g,Pb未检出,较电渗析前均有降低。电渗析对脱除褐藻胶的海带酶解液进行脱盐纯化处理,可有效地分离纯化出岩藻聚糖硫酸酯。     

岩藻聚糖硫酸酯的生物活性及作用机理研究进展

岩藻聚糖硫酸酯（Fucoidan）是一种含有硫酸酯的水溶性杂聚糖,是褐藻中特有的一种化学组分。研究发现岩藻聚糖硫酸酯在医学方面具有独特的功效,具有抗凝血、抗肿瘤、抗HIV、抗血栓、提高免疫力、降血脂等活性。综述了岩藻聚糖硫酸酯近几年在生物活性方面的研究进展。     

海带岩藻聚糖及其级分在氧化应激条件下对肉鸡巨噬细胞免疫功能的影响

【目的】在氧化应激条件下,研究海带岩藻聚糖及其级分对肉鸡巨噬细胞免疫功能的影响,初步探讨海带岩藻聚糖及其级分的免疫调节功能与抗氧化作用的关系。【方法】以叔丁基过氧化氢（tBOOH）为活性氧诱导剂,加入肉鸡腹腔巨噬细胞培养液中,测定细胞培养液中抗氧化酶的变化,巨噬细胞分泌一氧化氮（NO）、诱导型一氧化氮合成酶（iNOS）、以及细胞因子IL-1和TFN-α等免疫指标的变化。【结果】用tBOOH处理后的巨噬细胞,细胞存活率显著下降（P＜0.05）,乳酸脱氢酶（LDH）和丙二醛（MDA）显著升高（P＜0.05）,SOD和GSH-Px酶活性显著降低（P＜0.05）。巨噬细胞的吞噬活性显著降低（P＜0.05）,NO、iNOS和呼吸爆发显著降低（P＜0.05）,细胞因子IL-1分泌量显著下降（P＜0.05）,表明细胞出现明显的氧化损伤。在培养液中加入海带岩藻聚糖及其级分,能够缓解细胞的氧化应激,使得细胞存活率上升,LDH和MDA降低,SOD和GSH-Px升高,免疫指标均有不同程度的恢复。【结论】海带岩藻聚糖及其级分具有抗氧化活性,不同级分的抗氧化活性存在差异,其中级分Ⅲ、级分Ⅳ的作用较强。海带岩藻聚糖对巨噬细胞的免疫促进作用与其抗氧化活性有关。     

褐藻双寡糖（AFOD）和岩藻寡糖(FOS)预防草莓叶斑病的影响

本试验的目的是筛选出对草莓叶斑病有高效防治效果且绿色的防治方法。试验以“红颜”草莓品种为材料,分别采用不同浓度的褐藻双寡糖和岩藻寡糖单施以及与不同浓度的阿泰灵混合喷施,测定草莓的SPAD值和防治效果。结果表明,在整个生育期内70%褐藻双寡糖和岩藻寡糖能增加草莓叶片SPAD值,对草莓有促生长的作用,还可以预防草莓叶斑病,且高浓度70%褐藻双寡糖、岩藻寡糖与减量阿泰灵混用可提高阿泰灵的防治效果。     

两种寡糖类激发子诱导烟草抗烟草花叶病毒研究

对壳寡糖-铈配合物及褐藻酸钠寡糖进行诱导烟草抗TMV活性测定.结果发现,壳寡糖-铈配合物具有诱抗活性,最佳诱抗浓度为10 μg/mL,低于壳寡糖50 μg/mL.结果表明,褐藻酸钠寡糖具有诱抗活性,最佳诱抗浓度为25 μg/mL.     

Fucoidan sulfate promotes apoptosis of gastric cancer cells by regulating expression of HDAC1

AIM:To study the effects of fucoidan sulfate on the apoptosis of gastric cancer cells, and to explore its relationship with histone deacetylase 1 (HDAC1). METHODS:The effects of fucoidan sulfate on the viability of gastric cancer BGC-823 cells were measured by MTT assay. The cells were divided into si-HDAC1 group, si-NC group and fucoidan+pcDNA 3.1-HDAC1 group and fucoidan+pcDNA 3.1 group. The transfection were performed by liposome method. The apoptosis was analyzed by flow cytometry. The protein expression of HDAC1, Bcl-2 and Bax was determined by Western blot. The mRNA expression of HDAC1 was detected by RT-qPCR. RESULTS:Compared with the control cells, the inhibitory rates of the cell viability by fucoidan sulfate (0.2, 0.4, 0.6, 0.8 and 1.0 g/L) were increased signi-ficantly (P<0.05). The appropriate concentration was 0.6 g/L. Compared with control group, the expression of HDAC1 at mRNA and protein levels in fucoidan sulfate group was significantly down-regulated, while the apoptotic rate was significantly increased (P<0.05). Knock-down of HDAC1 expression significantly up-regulated the apoptotic rate, while over-expression of HDAC1 reversed the apoptosis-promoting effect of fucoidan sulfate on the BGC-823 cells. CONCLUSION:Fucoidan sulfate promotes apoptosis of gastric cancer cells. The mechanism may be related to the direct inhibition of HDAC1, which provides support for the clinical application of fucoidan sulfate.     

Effect of fucoidan on intestinal ischemia-reperfusion injury in rats

AIM:To investigate the effect and potential mechanism of fucoidan on intestinal ischemia-reperfusion (I/R) injury in rats. METHODS:Adult male Wistar rats were randomly divided into 3 groups:sham group, I/R group and Fucoidan+I/R group. Fucoidan at 160 mg/kg was intraperitoneally injected in rats of Fucoidan+I/R group 7 d prior to operation, and the equal volume of saline was intraperitoneally injected in rats of sham group and I/R group. The rats in I/R group and Fucoidan+I/R group underwent superior mesenteric artery occlusion for 1 h and then reperfusion for 2 h. Following reperfusion, the histomorphological changes of the ileum were examined by HE staining. The levels of diamine oxidase (DAO), D-lactic acid (D-LA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β were detected in the blood samples, the levels of malondialdehyde (MDA) and glutathione (GSH), the activity of superoxide dismutase (SOD) and myeloperoxidase (MPO), and the protein levels of Bax, cleaved caspase-3 and Bcl-2 were analyzed in intestinal tissue samples. RESULTS:Compared with sham group and Fucoidan+I/R group, the serum levels of DAO, D-LA, TNF-α, IL-6 and IL-1β were significantly increased in I/R group (P<0.05), Chiu's score of intestinal tissue, MDA content, MPO activity, the levels of Bax and cleaved caspase-3 protein in the intestinal tissues were also significantly increased (P<0.05), while the tissue GSH content, SOD activity, and Bcl-2 protein levels were significantly decreased (P<0.05). CONCLUSION:Fucoidan attenuates intestinal tissue damage caused by I/R, which may be related to anti-oxidation, anti-inflammatory and anti-apoptotic effects.     

海带岩藻聚糖及其级分对体外培养肉鸡巨噬细胞免疫功能的影响

 【目的】通过研究海带岩藻聚糖及其级分对肉鸡巨噬细胞免疫功能的影响,寻找海带提取物调节肉鸡免疫功能的有效级分,为饲料工业科学使用海带资源提供理论依据。【方法】采用水提醇沉的方法,从海带中提取岩藻聚糖,通过纤维柱和凝胶柱层析,对岩藻聚糖进行分级纯化。体外培养肉鸡腹腔巨噬细胞,在培养液中分别加入岩藻聚糖（200 μg•ml-1）和岩藻聚糖5种级分（100 μg•ml-1）,采用MTT方法检测细胞存活率,采用ELISA检测细胞因子IL-1和TNF-α,同时测定巨噬细胞的吞噬活性等其它免疫指标。【结果】海带岩藻聚糖及其级分显著提高肉鸡腹腔巨噬细胞的吞噬活性,促进巨噬细胞呼吸爆发、NO的产生量和iNOS活性,促进巨噬细胞分泌IL-1（P＜0.05）;海带岩藻聚糖不同级分对肉鸡巨噬细胞免疫功能的调控作用不同,其中级分Ⅲ和级分Ⅳ的促进作用较强,与对照组相比,可显著提高巨噬细胞的吞噬活性、呼吸爆发、NO产生量和iNOS活性。对其它指标无显著影响（P＞0.05）。【结论】海带岩藻聚糖及其级分可提高体外培养肉鸡腹腔巨噬细胞的免疫功能,不同级分对肉鸡巨噬细胞免疫功能的调控作用不同,其中级分Ⅲ和级分Ⅳ促进巨噬细胞免疫功能的作用最强,是海带岩藻聚糖中的有效级分。     

Effects of fucoidan on angiogenesis of human multiple myeloma RPMI 8226 cells

AIM: To investigate the effects of fucoidan on the angiogenesis of multiple myeloma cells in vitro, and its related mechanisms. METHODS: The human multiple myeloma RPMI 8226 cells and human endothelial cells were cultured in vitro. The growth inhibition rate of RPMI 8226 cells was examined by MTT assay. The cell cycle and apoptosis rate were measured by flow cytometry. RPMI 8226 cells were treated with fucoidan for 72 h, and the cell culture supernatant was collected. The VEGF concentration was examined by ELISA, and the tube formation assay was applied to assess the angiogenic activity. After treatment with fucoidan for 72 h at different concentrations, the protein levels of HIF-1α, VEGF, p-AKT and p-ERK1/2 were detected by Western blot. RESULTS: Fucoidan inhibited the growth of RPMI 8226 cells in a dose- and time-dependent manner. After treatment with fucoidan for 72 h, the cell cycle was arrested at G₁ phase, and the apoptotic rate of RPMI 8226 cells was increased with the increasing concentration of fucoidan, which was much higher than that in control group (P<0.05). The VEGF concentration was significantly decreased with the increa-sing concentration of fucoidan. The numbers and areas of the capillary-like structures decreased while the concentration of fucoidan increased, and those at 100 mg/L were less than those in the control (P<0.05). The protein levels of HIF-1α, VEGF, p-AKT and p-ERK1/2 in fucoidan group were significantly lower than those in control group (P<0.05). CONCLUSION: Fucoidan inhibits the secretion of VEGF in multiple myeloma cells, and reduces angiogenesis induced by multiple myeloma cells. It inhibits the protein expression of HIF-1α and VEGF, which may be related to inhibiting the phosphorylation of AKT and ERK1/2.