水溶性低聚壳聚糖、壳聚糖和山苍籽油抑菌效果比较

用固体培养基体外抑菌法,观察了不同浓度水溶性低聚壳聚糖、壳聚糖、山苍籽油对八叠球菌、枯草杆菌、大肠杆菌、放线菌5406及金黄色葡萄球菌生长的影响,并作抑菌动力学曲线.结果表明,随着时间延长,壳聚糖浓度在0.5%条件下,对5种细菌均能抑制;水溶性低聚壳聚糖在0.5%条件下对5种细菌也有不同程度的抑制作用;而山苍籽油对五种细菌均能抑制,但随着时间延长,效果减弱,可能与其有效成份为挥发性物质有关.     

水溶性壳聚糖的制备及其降血脂作用

目的研究水溶性壳聚糖的制备工艺,并考察其降血脂效果.方法采用H2O2氧化法制备水溶性壳聚糖,采用灌胃给药方式考察相对黏度为1.1、1.8和3.0(50℃条件)的水溶性壳聚糖对小白鼠降血脂药效.结果平均分子量1000壳聚糖的制备工艺条件为1%HAc为溶剂、壳聚糖浓度20 g/L、3%H2O2∶壳聚糖为0.5∶1、反应温度为60℃、反应时间为20 min.相对黏度为1.1、1.8和3.0的三种水溶性壳聚糖均能显著降低小鼠血浆的TCH水平,降幅可达26～30%.相对黏度1.1和3.0的壳聚糖能显著降低小鼠血浆的TG水平及MDA含量,降幅可分别达24～34%和38～40%.结论本工艺制备的三种不同黏度的壳聚糖具有较强的降脂药效,其降脂和抗氧化效果接近市售降脂良药软脉灵口服液.     

壳聚糖的超声波降解

目的 利用超声波将非水溶性的大分子壳聚糖降解为水溶性低分子量壳聚糖，优选降解的条件。方法 在稀醋酸溶液中，超声波的辐射作用下使壳聚糖发生降解，采用粘度测定法，探讨了超声波辐射时间与壳聚糖粘度的关系以及壳聚糖的浓度，醋酸的浓度对降解速度的影响。结果 壳聚糖浓度为1%左右，醋酸浓度为5-10%，降解速度最快，辐射7小时后粘度下降了73%，产物经高效液相色谱分析得知，随着超声波作用时间的延长低聚糖的含量逐渐增大，分子量也随之降低。结论 溶液中超声波降解壳聚糖是一种理想的有效降解方法。     

水溶性壳聚糖的制备及其降血脂作用

目的研究水溶性壳聚糖的制备工艺，并考察其降血脂效果。方法采用H₂O₂氧化法制备水溶性壳聚糖，采用灌胃给药方式考察相对黏度为1.1、1.8和3.0（50℃条件）的水溶性壳聚糖对小白鼠降血脂药效。结果平均分子量1000壳聚糖的制备工艺条件为：1%Hac为溶剂、壳聚糖浓度20 g/L、3%H₂O₂∶壳聚糖为0.5∶1、反应温度为60℃、反应时间为20 min。相对黏度为1.1、1.8和3.0的三种水溶性壳聚糖均能显著降低小鼠血浆的TCH水平，降幅可达26～30%。相对黏度1.1和3.0的壳聚糖能显著降低小鼠血浆的TG水平及MDA含量，降幅可分别达24～34%和38～40％。结论本工艺制备的三种不同黏度的壳聚糖具有较强的降脂药效，其降脂和抗氧化效果接近市售降脂良药软脉灵口服液。     

水溶性壳聚糖对肝癌细胞生长抑制的实验研究

目的 观察壳聚糖对肝癌细胞SMMC7721的生长抑制作用.方法 采用MTT法研究了不同浓度水溶性壳聚糖对肝癌细胞株SMMC7721的生长抑制作用.结果 水溶性壳聚糖可抑制肝癌细胞的生长,在一定范围内(50～400mg/L)呈剂量依赖关系.结论 水溶性壳聚糖对肝癌细胞的生长有抑制,并且呈剂量依赖关系.     

水溶性壳聚糖抗肿瘤作用的实验研究

目的研究水溶性壳聚糖对抗肿瘤活性因子和NK细胞活性的影响。方法分别用不同浓度水溶性壳聚糖腹腔注射荷瘤小鼠 ,然后测定巨噬细胞一氧化氮 (NO)、肿瘤坏死因子 (TNF)的生成 ,以及脾细胞γ 干扰素(IFN γ)和NK细胞活性。结果水溶性壳聚糖有显著地促进荷瘤小鼠NO、TNF、IFN γ的生成 ,提高NK细胞活性。与对照相比P <0 .0 1。结论水溶性壳聚糖能提高荷瘤小鼠的免疫功能。     

阿司匹林/壳聚糖聚集体的形成和释放行为

摘 要：目的 探究阿司匹林对壳聚糖聚集体形成的影响以及阿司匹林/壳聚糖聚集体对阿司匹林的释放性能。方法 选用浓度为0.25 mol/L和0.3 mol/L的柠檬酸溶解壳聚糖并绘制柠檬酸/壳聚糖/温度二元相图。利用阿司匹林与壳聚糖构筑聚集体并进行稳态扫描,测定其流变性质。选用壳聚糖质量分数为2.5 %和5.0 %的聚集体作为阿司匹林的药物载体进行体外释放,对释放过程进行动力学拟合。结果 稳态流变表明阿司匹林/壳聚糖聚集体有较强的假塑性。释放实验中,阿司匹林的释放过程符合一级动力学方程,通过对空白样品对比,四组聚集体对阿司匹林均有缓释效果。结论 利用阿司匹林与柠檬酸溶解的壳聚糖构筑的聚集体对药物阿司匹林有着良好的缓释效果。其中柠檬酸浓度为0.3 mol/L,壳聚糖质量百分数为5.0 %的聚集体包载阿司匹林时,达到最大释放量的时间为10 h。     

壳聚糖及其衍生物对肝癌细胞SMMC7721的生长抑制作用

目的观察壳聚糖及其衍生物对肝癌细胞SMMC7721的生长抑制作用。方法采用四甲基偶氮唑盐(MTT)法研究了不同浓度水溶性壳聚糖、磺化壳聚糖、羧甲基壳聚糖和壳寡糖对肝癌细胞株SMMC7721的生长抑制作用。结果在4种不同壳聚糖及其衍生物中,水溶性壳聚糖和磺化壳聚糖可显著抑制肝癌细胞的生长,并在一定范围内(50~400 mg/L)呈剂量依赖关系,其中以磺化壳聚糖最为显著,羧甲基壳聚糖和壳寡糖对肝癌细胞无生长抑制作用。结论壳聚糖及其衍生物可抑制肝癌细胞的生长,并且呈剂量依赖关系。     

Box-Behnken响应面法优化水溶性壳聚糖对黄莪凝胶水提液的除杂工艺

目的:优化水溶性壳聚糖对黄莪凝胶水提液除杂的工艺条件。方法:以透光率比、杂质去除率、柚皮苷保留率的综合评分为指标,采用Box-Behnken响应面法优化除杂工艺中水溶性壳聚糖用量、振荡时间和温度,并进行验证。结果:比重≥1.3的中药水提液与0.01 g/mL水溶性壳聚糖溶液用量的体积比为2.2,70℃下振荡100 min除杂效果最佳;验证试验中3批样品的平均透光率比为87.3%、杂质去除率为41.50%、柚皮苷保留率为131.38%,综合评分的实测值分别为97.35%、98.92%、98.04%,与预测值(98.27%)的相对误差分别为-0.87%、0.73%、-0.16%。结论:该方法可有效优化水溶性壳聚糖对黄莪凝胶水提液的除杂工艺参数。     

壳聚糖-阿拉伯胶布洛芬缓释微囊制备工艺初探

本文以壳聚糖和阿拉伯胶为囊材,采用复凝法将非甾族抗炎药布洛芬微囊化。探索了不同pH值、不同壳聚糖浓度、不同搅拌转速、不同成囊温度、不同浓度戊二醛固化交联剂对微囊制备工艺的影响:研究表明在PH值=4.0,壳聚糖浓度为0.3%,搅拌转速为200r·min-1,成囊温度为45℃,戊二醛用量为25%,1.0mL时制备的缓释微囊;具有囊型好、粒径分布均匀,包封率高且制备工艺稳定。     

Synthesis,Cytotoxicity and Antileishmanial Activity of Some N-(2-(indol-3-yl)ethyl)-7-chloroquinolin-4-amines

We report herein the condensation of 4,7-dichloroquinoline (1) with tryptamine (2) and D-tryptophan methyl ester (3) . Hydrolysis of the methyl ester adduct (5) yielded the free acid (6) . The compounds were evaluated in vitro for activity against four different species of Leishmania promastigote forms and for cytotoxic activity against Kb and Vero cells. Compound (5) showed good activity against the Leishmania species tested, while all three compounds displayed moderate activity in both Kb and Vero cells.     

Lung disease and PKCs

The lung offers a rich opportunity for development of therapeutic strategies focused on isozymes of protein kinase C (PKCs). PKCs are important in many cellular responses in the lung, and existing therapies for pulmonary disorders are inadequate. The lung poses unique challenges as it interfaces with air and blood, contains a pulmonary and systemic circulation, and consists of many cell types. Key structures are bronchial and pulmonary vessels, branching airways, and distal air sacs defined by alveolar walls containing capillaries and interstitial space. The cellular composition of each vessel, airway, and alveolar wall is heterogeneous. Injurious environmental stimuli signal through PKCs and cause a variety of disorders. Edema formation and pulmonary hypertension (PHTN) result from derangements in endothelial, smooth muscle (SM), and/or adventitial fibroblast cell phenotype. Asthma, chronic obstructive pulmonary disease (COPD), and lung cancer are characterized by distinctive pathological changes in airway epithelial, SM, and mucous-generating cells. Acute and chronic pneumonitis and fibrosis occur in the alveolar space and interstitium with type 2 pneumocytes and interstitial fibroblasts/myofibroblasts playing a prominent role. At each site, inflammatory, immune, and vascular progenitor cells contribute to the injury and repair process. Many strategies have been used to investigate PKCs in lung injury. Isolated organ preparations and whole animal studies are powerful approaches especially when genetically engineered mice are used. More analysis of PKC isozymes in normal and diseased human lung tissue and cells is needed to complement this work. Since opposing or counter-regulatory effects of selected PKCs in the same cell or tissue have been found, it may be desirable to target more than one PKC isozyme and potentially in different directions. Because multiple signaling pathways contribute to the key cellular responses important in lung biology, therapeutic strategies targeting PKCs may be more effective if combined with inhibitors of other pathways for additive or synergistic effect. Mechanisms that regulate PKC activity, including phosphorylation and interaction with isozyme-specific binding proteins, are also potential therapeutic targets. Key isotypes of PKC involved in lung pathophysiology are summarized and current and evolving therapeutic approaches to target them are identified.     

Gender-related symptoms and correlates of alcohol dependence among men and women with a lifetime diagnosis of alcohol use disorders

This study explored gender-related symptoms and correlates of alcohol dependence in a crosssectional study of 150 men and 150 women with a lifetime diagnosis of alcohol use disorders (AUD). Participants were recruited in equal numbers from treatment settings, correctional centres and the general community. Standardized measures were used to determine participants' use of substances, history of psychiatric disorders and psychosocial stress, their sensation seeking and family history of substance use and mental health disorders. Multivariate analyses were used to detect patterns of variables associated with gender and the lifetime severity of AUD. Men had a longer history of severe AUD than women. Women had similar levels of alcohol dependence and medical and psychological sequelae as men, despite 6 fewer years of AUD. More women than men had a history of severe psychosocial stress, severe dependence on other substances and antecedent mental health problems, especially mood and anxiety disorders. There were differences in family history of alcohol-related problems approximating same-gender aggregation. The severity of a lifetime AUD was predicted by its earlier age at onset and the occurrence of other disorders, especially anxiety, among both men and women. The limitations in the generalizability of these findings due to sample idiosyncrasies are discussed.     

Biochemical and molecular characterisation of cubozoan protein toxins

Class Cubozoa includes several species of box jellyfish that are harmful to humans. The venoms of box jellyfish are stored and discharged by nematocysts and contain a variety of bioactive proteins that are cytolytic, cytotoxic, inflammatory or lethal. Although cubozoan venoms generally share similar biological activities, the diverse range and severity of effects caused by different species indicate that their venoms vary in protein composition, activity and potency. To date, few individual venom proteins have been thoroughly characterised, however, accumulating evidence suggests that cubozoan jellyfish produce at least one group of homologous bioactive proteins that are labile, basic, haemolytic and similar in molecular mass (42-46 kDa). The novel box jellyfish toxins are also potentially lethal and the cause of cutaneous pain, inflammation and necrosis, similar to that observed in envenomed humans. Secondary structure analysis and remote protein homology predictions suggest that the box jellyfish toxins may act as α-pore-forming toxins. However, more research is required to elucidate their structures and investigate their mechanism(s) of action. The biological, biochemical and molecular characteristics of cubozoan venoms and their bioactive protein components are reviewed, with particular focus on cubozoan cytolysins and the newly emerging family of box jellyfish toxins.     

Dose tolerability of chronically inhaled voriconazole solution in rodents

Invasive pulmonary aspergillosis (IPA) is a fungal disease of the lung associated with high mortality rates in immunosuppressed patients despite treatment. Targeted drug delivery of aqueous voriconazole solutions has been shown in previous studies to produce high tissue and plasma drug concentrations as well as improved survival in a murine model of IPA. In the present study, rats were exposed to 20 min nebulizations of normal saline (control group) or aerosolized aqueous solutions of voriconazole at 15.625 mg (low dose group) or 31.25 mg (high dose group). Peak voriconazole concentrations in rat lung tissue and plasma after 3 days of twice daily dosing in the high dose group were 0.85 ± 0.63 μg/g wet lung weight and 0.58 ± 0.30 μg/mL, with low dose group lung and plasma concentrations of 0.38 ± 0.01 μg/g wet lung weight and 0.09 ± 0.06 μg/mL, respectively. Trough plasma concentrations were low but demonstrated some drug accumulation over 21 days of inhaled voriconazole administered twice daily. Following multiple inhaled doses, statistically significant but clinically irrelevant abnormalities in laboratory values were observed. Histopathology also revealed an increase in the number of alveolar macrophages but without inflammation or ulceration of the airway, interstitial changes, or edema. Inhaled voriconazole was well tolerated in a rat model of drug inhalation.