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1.
不同相对分子质量壳聚糖的制备和部分性质研究   总被引:2,自引:1,他引:2  
目的制备不同相对分子质量 (Mr)壳聚糖并研究其部分性质。方法在中性条件下 ,用过氧化氢氧化法制备不同Mr 的壳聚糖 ,并进行红外表征、热分析和稳定性等研究。结果探索到制备不同Mr 壳聚糖的最适宜条件。结论壳聚糖经过氧化氢降解后 ,结构没有明显变化 ,且随壳聚糖Mr 的降低 ,其稳定性增强  相似文献   

2.
过氧化氢氧化降解法制备低分子玻璃酸   总被引:4,自引:0,他引:4  
目的制备低分子玻璃酸 (HA)。方法过氧化氢氧化降解法。结果随着过氧化氢浓度增加 ,反应温度的升高 ,降解速率加快。中性条件下HA的氧化降解速率较快 ,而酸性或碱性时却较慢。为了方便降解过程的可控性 ,过氧化氢浓度选 0 .0 5 % ,反应温度定为 5 0℃ ,反应pH为中性。随着HA相对分子质量的降低 ,运动黏度迅速下降 ,而糖醛酸含量基本不变。不同过氧化氢浓度降解时 ,低分子HA收率基本相同。结论过氧化氢氧化降解法可用于制备低分子HA。  相似文献   

3.
微波辐射快速制备水溶性壳聚糖   总被引:18,自引:1,他引:17  
目的快速制备水溶性壳聚糖。方法利用微波辐射 ,用过氧化氢作氧化剂 ,非均相降解高分子量壳聚糖。设计了正交试验法 ,得到最优化反应条件。结果最优反应条件为 5 %过氧化氢、5 %壳聚糖 ,微波辐射功率约40 0W ,辐射 3min ,所得水溶性壳聚糖分子量为 1 .1× 1 0 4 D ,收率可达 60 %。结论微波法制备低聚壳聚糖效果理想 ,可进一步扩展到壳聚糖的其它化学修饰  相似文献   

4.
一种低分子壳聚糖硫酸酯铝的制备   总被引:6,自引:2,他引:4  
本文采用正交试验设计方法对壳聚糖进行氧化降解,获得了一种低相对分子质量的水溶性壳聚糖,并在此基础上经硫酸化和盐交换制得了一种低相对分子质量壳聚糖硫酸酯式铝盐,壳聚糖氧化降解实验结果表明降解的最佳条件是温度为80度,过氧化氢浓度为5%,降解时间为1h,在此条件一产品收率可达52.68%,其粘均相对分子质量为3990,对制是的低相对分子质量壳聚糖硫酸酯铝进行了红外光谱分析和部分理化性质测定,经测定定样品中有机硫(S)含量为9.10%,铝(Al)含量为20.58%,样品制酸力为188.59mL.g^-1。  相似文献   

5.
溶菌酶对壳聚糖降解的研究   总被引:6,自引:0,他引:6  
对溶菌酶降解壳聚糖的过程进行了研究。探讨了降解过程的粘度变化、温度、pH值、反应时间、酶浓度、壳聚糖浓度以及壳聚糖的脱乙酰化度对酶促反应速度的影响。实验结果表明,以壳聚糖为底物的溶菌要不得的催化是属米氏酶的特征,该酶促反应的最适宜温度为50℃,适宜pH值是6.0左右,壳聚糖的脱乙酰度越低降解速度越快。产品经高效液相色谱测定相对分子质量低于1万,相对分子质量组分集中,水溶性良好。  相似文献   

6.
蜗牛酶降解壳聚糖制备壳寡糖的研究   总被引:1,自引:0,他引:1  
目的 研究筛选蜗牛酶降解壳聚糖的最佳反应条件.方法 采用正交试验法,以降解产物中寡糖的量和糖收率为指标,考察温度、酶浓度、pH对蜗牛酶降解壳聚糖的影响,筛选最佳反应条件;采用SDS-PAGE检测降解产物,用改良Schales法测定还原糖的含量并计算寡糖的收率.结果 蜗牛酶降解壳聚糖的最佳反应条件为:pH4、40℃、酶底比为8:100.最佳条件下的寡糖收率为64.74%,产物主要是聚合度为4以上的寡糖.结论 在最佳反应条件下,蜗牛酶能较好地降解壳聚糖.  相似文献   

7.
四种不同类型酶降解壳聚糖的效果比较   总被引:8,自引:0,他引:8  
目的:对4种不同类型酶水解壳聚糖的效果进行比较。方法:通过碱性铁氰化钾测定还原端基法测定了酶活性和溶液中还原糖浓度,研究并评价了纤维素酶、脂肪酶、溶菌酶和胃蛋白酶对壳聚糖溶液的降解条件和效果。结果:分别在4种酶的最适宜条件下反应,胃蛋白酶对壳聚糖水解速度最快,纤维素酶的水解速度仅次于胃蛋白酶,溶菌酶的水解速度最慢。结论:胃蛋白酶对壳聚糖的降解速度优于纤维素酶、脂肪酶和溶菌酶。  相似文献   

8.
甲壳低聚糖的制备和分析   总被引:44,自引:10,他引:34  
解决壳聚精的水不溶性,拓宽壳聚精的应用范围。方法:直接用过氧化氢对高分子量、高脱乙酸化度的壳聚糖进行非均相降解、制备了水溶性甲壳低聚糖产品,对产品进行红外光谱结构表征,并用高效毛细管电泳测定了寡糖的聚合度。探讨了温度、过氧化氢浓度对降解所需时间、产品得率及甲壳低聚糖聚合度的影响。结果:选择降解温度 80℃~90℃,过氧化氢浓度 8%~10%时,水解时间0.5 ~1.0 h,水溶性产品得率为 40%~45%,聚合度为3~7的寡糖占水解产物的36%~50%。结论:该方法制备甲壳低聚糖是可行的。如进一步研究工艺条件,有望进行工业化生产。  相似文献   

9.
目的:介绍水溶性壳聚糖的主要生物活性和制备方法,为水溶性壳聚糖的合理利用和开发提供参考。方法:根据国内、外文献资料进行归纳、分析、加以综述。结果:壳聚糖具有无毒、免疫、可生物降解的性质,水溶性低分子量壳聚糖的抑菌、抑制肿瘤、抗疲劳和抗氧化能力显著增强。选择降解方法和所需壳聚糖分子量有关,可使用绿色降解法、氧化降解法和酶物理降解法制备水溶性壳聚糖。结论:通过各种降解方法所得到的水溶性低分子量壳聚糖是1种具有高生物活性的生物材料或潜在药物。  相似文献   

10.
改性壳聚糖膜在兔眼中的降解及组织病理学观察   总被引:3,自引:1,他引:3  
目的了解兔眼中壳聚糖膜的降解与生物相容性 ,观察眼组织的病理学变化。方法对兔眼实施小梁切除术 ,将不同相对分子质量改性壳聚糖膜 ,植入板层巩膜瓣下 ,分别于术后 1、4、1 2周处死 ,摘除眼球 ,病理切片 ,观察组织反应。结果在植入早期 1、4周时 ,局部组织出现明显的炎症反应 ,随时间的推移 ,改性壳聚糖膜的降解速度加快 ,1 2周时 ,已降解为碎屑状 ,炎症反应基本消失。结论改性壳聚糖膜植入兔眼内可降解吸收 ,对兔眼组织不产生病理性损害  相似文献   

11.
There is an increasing evidence that oxidative stress is implicated in the processes of inflammation and carcinogenesis. It has been shown that kahweol and cafestol, coffee-specific diterpenes, exhibit chemoprotective effects. This study investigated the effects of kahweol and cafestol, coffee-specific diterpenes, on the hydrogen peroxide (H(2)O(2))-induced oxidative stress and DNA damage in NIH3T3 cells. When the cells were treated with kahweol or cafestol, cytotoxicity, lipid peroxidation, and reactive oxygen species production induced by H(2)O(2) were markedly reduced in a dose-dependent manner. Moreover, kahweol and cafestol were shown to be highly protected against H(2)O(2)-induced oxidative DNA damage as determined by the Comet (single cell gel electrophoresis) assay and the measurement of 8-oxoguanine content in NIH3T3 cells. Kahweol and cafestol also protected hydroxyl radical-induced 2-deoxy-d-ribose degradation by ferric ion-nitrilotriacetic acid and H(2)O(2). In addition, kahweol and cafestol efficiently removed the superoxide anion generated from the xanthine/xanthine oxidase system. These results suggest that kahweol and cafestol are effective in protecting against H(2)O(2)-induced oxidative stress and DNA damage, probably via scavenging free oxygen radicals, and that kahweol and cafestol act as antioxidants.  相似文献   

12.
1-(4-Methoxyphenylethyl)-11H-benzo[f]-1,2-dihydro-pyrido[3,2,c][1,2,5]oxathiazepine 5,5 dioxide (BZN) is a cytotoxic derivative with very promising in vitro activity. Regulatory authority for registration of pharmaceuticals for human use requires to evaluate the stability of active compound under various stress conditions. Forced degradation of BZN was investigated under hydrolytic (0.1M NaOH, 0.1M HCl, neutral), oxidative (3.3% H(2)O(2)), photolytic (visible light) and thermal (25 °C, 70 °C) settings. Relevant degradation took place under thermal acidic (0.1M HCl, 70 °C) and oxidative (3.3% H(2)O(2)) conditions. Liquid chromatography-mass spectrometry (LC-MS) analyses revealed the presence of ten degradation products whose structures were characterized by electrospray ionization-orbitrap mass spectrometry. The full scan accurate mass analysis of degradation products was confirmed or refuted using three tools furnished by the MS software: (1) predictive chemical formula and corresponding mass error; (2) double bond equivalent (DBE) calculation; and (3) accurate mass product ion spectra of degradation products. The structural elucidation showed that the tricycle moiety was unstable under thermal acidic and oxidative conditions since four degradation products possess an opened oxathiazepine ring. Then, a simple and fast HPLC-UV method was developed and validated for the determination of the degradation kinetic of BZN under acidic and oxidative conditions. The method was linear in the 5-100 μg mL(-1) concentration range with a good precision (RSD=2.2% and 2.7% for the repeatability and the intermediate precision, respectively) and a bias which never exceeded 1.6%, whatever the quality control level. With regards to the BZN concentration, a first-order degradation process was determined, with t(1/2)=703 h and 1140 h, under oxidative and acidic conditions, respectively.  相似文献   

13.
去甲斑蝥二羧酸壳聚糖络合物的制备及药理活性研究   总被引:1,自引:0,他引:1  
目的:制备去甲斑蝥二羧酸壳聚糖络合物(NCTD络合物),降低去甲斑蝥素的毒性,增强抗肿瘤活性。方法:应用间歇式碱性水解得到的高脱乙酰度(DD)壳聚糖与去甲斑蝥二羧酸制备络合物,通过小鼠尾静脉、灌胃方式分别观察络合物与去甲斑蝥素的急性毒性,计算半数致死量(median lethal dose,LD_(50));建立小鼠移植性H_(22)肝癌肿瘤模型,观察NCTD络合物对肿瘤生长的抑制作用。结果:NCTD络合物能降低去甲斑蝥素的毒性;络合物的低、中、高剂量组均抑制小鼠的肿瘤生长,抑瘤率分别达26.60%、31.69%、44.38%,呈量效关系。结论:去甲斑蝥二羧酸与壳聚糖所成的络合物增加了水溶性,降低了毒性,提高了疗效。  相似文献   

14.
We recently developed two biomarker sets for oxidative damage: one for determination of lipid peroxidation (LPO) degradation products; acetaldehyde, propanal, butanal, pentanal, hexanal, heptanal, octanal, nonanal, malondialdehyde and acetone, by a gas chromatography-electron capture detection method, and the other for protein oxidation products such as o,o'-dityrosine, by an isotope dilution high performance liquid chromatography-tandem mass spectrometry method. In the present study, we explored the possibility to utilize these biomarkers for determining the oxidative damage in liver mammalian cells in vitro. Two different treatments were chosen for inducing oxidative stress in Chinese Hamster ovary cells: menadione and copper plus hydrogen peroxide (Cu2+/H2O2). Cells were incubated with the model compounds in the presence or absence of vitamin E and C, and cytotoxicity was evaluated by a nuclear-dye method. Results were compared to two fluorescent probes, H2DCF-DA and C11 -BODIPY581/591, which have been used for determining the formation of free radicals in the cells. From ten LPO degradation products, eight were increased significantly following incubation with menadione in cell lysate or incubation media. Menadione-induced oxidative stress was also confirmed by oxidation of fluorescent probes. However, no increased formation of protein oxidation products was observed. Vitamin E and C did not diminish the formation of LPO degradation products that were increased by menadione. Although Cu2+/H2O2 did not induce oxidation of fluorescent probes, it induced formation of six out of ten LPO degradation products. Vitamin E and C did not diminish the formation of LPO degradation products; vitamin C even substantially increased the formation of acetaldehyde and propanal, which is in line with its reported prooxidant action under certain conditions. Vitamin C also caused two-fold increase in Cu2+/H2O2-induced o,o'-dityrosine formation when applied simultaneously. In conclusion, our present results show that the LPO biomarker set can be used for evaluation of oxidant capacity and the toxic potential of various chemicals in an in vitro cell model. These biomarkers might even be more sensitive than measuring protein oxidation products or oxidation of fluorescent probes.  相似文献   

15.
低聚氨基葡萄糖的研制   总被引:11,自引:0,他引:11  
在中性条件下采用双氧水对脱乙酰壳多糖进行氧化降解,制备了分子量为1000左右的药用低聚氨基葡萄糖。讨论了不同的双氧水浓度,配比,温度和反应时间对降解反应的影响,并用傅立叶红外分析表征了产物的结构。  相似文献   

16.
The evaluation of N-trimethyl chitosan (TMC)-coated liposomes containing Coenzyme Q(10) as potential ophthalmic drug delivery system was carried out. Firstly, transcorneal permeation studies were conducted at 34°C using a side-by-side diffusion apparatus. The transport process of the fluorescent marker, rhodamine B, across the corneal epithelium was visualized with confocal laser scanning microscopy. Secondly, the human lens epithelial cells (HLECs) were cultured without or with Coenzyme Q(10) followed by addition of H(2)O(2). The cell viability and apoptosis were evaluated. The permeability coefficient for rhodamine B with TMC-coated liposomes increased more than two times in comparison with the value obtained for solution as control, from (0.42±0.018)×10(5)cms(-1) to (1.31±0.030)×10(5)cms(-1). Confocal laser scanning microscopy revealed that a TMC coating enhanced the transepithelial transport, dependent on the TMC concentration and contacting time. Coenzyme Q(10) elevated the cell viability and reduced the oxidative damage with the decreased percentage of apoptotic cells in a positive concentration-dependent manner. The ATP content of liposome-treated cells was increased about 2-fold compared with that of H(2)O(2)-treated cells. Together, our findings demonstrate that with the enhanced permeation effect of the TMC coating, Coenzyme Q(10)-loaded TMC-coated liposomes appear to be a promising ophthalmic drug delivery carrier with an efficacy in protecting HLECs against H(2)O(2)-induced oxidative damage.  相似文献   

17.
Quercetin possesses a broad range of pharmacological properties, including protection of LDL from oxidation. However, little is known about the mechanism by which quercetin rescues cardiomyoblasts from oxidative damage. This study was designed to investigate the protective mechanism of quercetin on H(2)O(2)-induced toxicity of H9c2 cardiomyoblasts. Oxidative stress, such as H(2)O(2), ZnCl(2), and menadione, significantly decreased the viability of H9c2 cells, which was accompanied with apparent apoptotic features, including fragmentation of genomic DNA as well as activation of caspase protease. However, quercetin markedly inhibited the apoptotic characteristics via reduction of intracellular reactive oxygen species generation. Also, it prevented the H(2)O(2)-mediated mitochondrial dysfunction, including disruption of mitochondria membrane permeability transition as well as an increase in expression of apoptogenic Bcl-2 proteins, Bcl-2 and Bcl-X(L). Furthermore, pretreatment of quercetin inhibited the activation of caspase-3, thereby both cleavage of poly(ADP-ribose) polymerase and degradation of inhibitor of caspase-activated DNase/DNA fragmentation factor by H(2)O(2) were completely abolished. Taken together, these data suggest that protective effects of quercetin against oxidative injuries of H9c2 cardiomyoblasts may be achieved via modulation of mitochondrial dysfunction and inhibition of caspase activity.  相似文献   

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