两种聚(左旋乳酸-己内酯)静电纺纳米纤维膜的性能比较

背景：聚左旋乳酸和聚己内酯各自都有其优点与缺点,而共聚或共混后性能可以得到有效的改善,但因为两者添加比例的不同会对性能有一定的影响,在不同的纺丝溶液浓度下纺出的纤维性能亦会有所差异。 目的：通过对两种原料聚(左旋乳酸-己内酯) (75/25;50/50)在不同纺丝液浓度下制得的纳米纤维膜各种性能的比较,选出最佳的原料和相应的纺丝液浓度。 设计、时间及地点：对比观察实验,于2007-09/2008-11在东华大学生物材料与组织工程实验室完成。 材料：将聚聚(左旋乳酸-己内酯)材料在乳酸/己内酯为75/25和50/50两种比例下,在质量分数为4%,6%,8%和10%纺丝液浓度下通过静电纺丝制备纳米纤维膜。 方法：扫描电镜样品经表面喷金后在10 kV加速电压下观察纤维膜的形貌。在万能材料测试机测试其断裂强度和断裂伸长率。采用MTT法测试猪髋动脉内皮细胞在纳米纤维膜上的黏附与增殖情况。 主要观察指标：静电纺纳米纤维膜的纤维形态、力学性能及生物相容性。 结果：通过扫描电镜观察发现由质量分数为6%聚(左旋乳酸-己内酯) (50/50)制备的纤维膜具有更好的纤维形态,且直径分布均匀;拉伸力学测试显示由聚(左旋乳酸-己内酯) (50/50)制备的纤维膜比聚(左旋乳酸-己内酯) (75/25)具有更高的断裂伸长率,但断裂应力较低;细胞生物相容性实验表明猪髋动脉内皮细胞在质量分数为6%和8%聚(左旋乳酸-己内酯) (50/50)的纳米纤维膜上更能有效的黏附与增殖。 结论：纺丝液质量分数为6%的聚(左旋乳酸-己内酯) (50/50)制得的纳米纤维膜各项性能较优。     

Fe3O4磁性微粒的制备及表征

背景：磁性微粒作为一种磁性载体在固定化酶、免疫检测、靶向载药治疗及细胞分离等生物医学领域得到了广泛的应用。 目的：制备分散稳定性好,相对磁性强的纳米级Fe3O4微粒。 方法：以氯化亚铁、氯化铁、氢氧化钠为主要原料,采用化学共沉淀法合成Fe3O4磁性粒子。 结果与结论：用正交设计法优化了Fe3O4微粒的合成工艺条件,得到制备Fe3O4粒子的最佳实验条件为Fe2+/Fe3+的物质的量之比为2∶1、共沉淀时的pH值为11、熟化温度为90 ℃、表面活性剂聚乙二醇的用量为40 mL,此时制得的Fe3O4粒子粒径最小,为78 nm,Fe3O4溶液的分散稳定性最好,相对磁性最强。从Fe3O4的扫描电镜图可以看出,Fe3O4微粒晶体颗粒为纳米级。     

电纺丝聚乳酸、聚3羟基丁酸酯共聚4羟基丁酸酯和聚碳酸亚丙酯纳米纤维的制备及表面亲水性

背景：近年来聚乳酸、羟基磷灰石类复合材料支架具有良好的生物降解性和生物相容性而被广泛的研究,但是这类复合材料在增强材料界面的结合、调节材料的降解速率、改善材料的强度等方面仍不能满足理想的组织工程支架材料的要求。 目的：探讨电纺丝法制备纳米纤维的结构形态及表面亲水性。 方法：分别将聚乳酸、聚3羟基丁酸酯共聚4羟基丁酸酯和聚碳酸亚丙酯通过静电纺丝法制备纳米纤维膜,扫描电镜对纤维膜的结构形态进行分析,并观察在人体环境相近的磷酸盐缓冲溶液(37 ℃,pH 7.4)中浸泡不同时间的表面亲水性。 结果与结论：通过静电纺丝技术可以将聚乳酸、聚3羟基丁酸酯共聚4羟基丁酸酯和聚碳酸亚丙酯3种材料制备成微纳米纤维结构,控制制备参数可以获得不同直径的纤维,样品随着在培养液中的浸泡时间延长,总体显示出接触角比初始降低,亲水性增强。 关键词：聚乳酸;聚3羟基丁酸酯共聚4羟基丁酸酯;聚碳酸酯;电纺丝;亲水性 doi:10.3969/j.issn.1673-8225.2010.12.046     

载TK 基因PEG-PEI Fe3O4纳米磁流体的制备及其相关性质*

目的：制备载pAFP-TK基因PEG-PEI Fe3O4纳米磁流体并探讨其相关特性。 方法：用化学共沉淀法制备PEG-PEI Fe3O4纳米磁流体,将pAFP-TK自杀基因表达质粒包裹,形成载TK基因的PEG-PEI Fe3O4纳米磁流体。 结果：粒径分析仪及原子力显微镜检测载TK基因PEG-PEI Fe3O4纳米磁流体平均粒径202.6 nm,分布均匀,无黏附团聚。琼脂糖凝胶电泳分析PEG-PEI Fe3O4纳米磁流体与DNA比例达10∶1时,结合率最高,达93.56%。PEG-PEI Fe3O4纳米磁流体中的DNA在37 ℃、DNaseI及血清存在下消化数小时后,仍然保持结构的完整。 结论：载pAFP-TK基因表达质粒的PEG-PEI Fe3O4纳米磁流体与DNA有较高的结合率,可以有效地保护质粒DNA等特性。     

Involvement of dopamine D(2)/D(3) receptors and BDNF in the neuroprotective effects of S32504 and pramipexole against 1-methyl-4-phenylpyridinium in terminally differentiated SH-SY5Y cells

Anti-parkinsonian agents possessing both D(2) and D(3) receptor agonist properties are neuroprotective against 1-methyl-4-phenylpyridinium (MPP(+)) toxicity in a variety of in vitro models. The mechanisms underlying protection by these D(2)/D(3) receptor agonists remain poorly defined. To test if the D(3) receptor preferring agonists S32504 and pramipexole act through D(2) or D(3) receptors and via brain-derived neurotrophic factor (BDNF)-dependent pathways, we utilized a terminally differentiated neuroblastoma SH-SY5Y cell line exhibiting a dopaminergic phenotype. The cytotoxic effects of MPP(+) (LD(50) of 100 microM) were stereospecifically antagonized by S32504 (EC(50) = 2.0 microM) and, less potently, by pramipexole (EC(50) = 64.3 microM), but not by their inactive stereoisomers, R(+) pramipexole and S32601, respectively. Neuroprotective effects afforded by EC(50) doses of S32504 and pramipexole were antagonized by the selective D(3) antagonists S33084, U99194A, and SB269652, and by the D(2)/D(3) antagonist raclopride. However, the preferential D(2) receptor antagonist LY741626 was ineffective as was the D1 antagonist SCH23390. BDNF (1 nM) potently protected against MPP(+)-induced neurotoxicity. Antibody directed against BDNF concentration-dependently blocked both the neuroprotective effects of BDNF and those of pramipexole and S32504 against MPP(+). The protection afforded by BDNF was blocked by the P3K-AKT pathway inhibitor LY249002 and less so by the MEK/MAPKK pathway inhibitor PD98059. LY249002, but not PD98059, blocked the neuroprotective effects of pramipexole and S32504 against MPP(+) toxicity. In conclusion, S32504 and, less potently, pramipexole show robust, stereospecific, and long-lasting neuroprotective effects against MPP(+) toxicity that involve D(3) receptors. Their actions also reflect downstream recruitment of BDNF and via a PK3-AKT pathway.     

Role of the amygdaloid cholecystokinin (CCK)/gastrin-2 receptors and terminal networks in the modulation of anxiety in the rat. Effects of CCK-4 and CCK-8S on anxiety-like behaviour and [3H]GABA release

The amygdala plays a key role in fear and anxiety. The intercalated islands are clusters of glutamate-responsive GABAergic neurons rich in cholecystokinin (CCK)-2 receptors which control the trafficking of nerve impulses from the cerebral cortex to the central nucleus of amygdala. In this study, the nature of the CCK–glutamate–GABA interactions within the rat rostral amygdala, and their relevance for anxiety, were studied. CCK/gastrin-like immunoreactive nerve terminals were found to be mainly restricted to the paracapsular intercalated islands and the rostrolateral part of the main intercalated island. Behaviourally, the bilateral microinjection of CCK-4 (0.043–4.3 pmol/side) or CCK-8S (4.3 pmol/side) into the rostrolateral amygdala reduced the open-arm exploration in the elevated plus-maze without affecting locomotion. In contrast, neither CCK-4 nor CCK-8S (0.043–4.3 pmol/side) had any effects in the shock-probe burying test as compared with their saline-treated controls. Biochemically, CCK-4 (0.3 and 1.5 µ m ), unlike CCK-8S, enhanced significantly the K⁺-stimulated release of [³H]GABA from amygdala slices. These effects were fully prevented by prior superfusion of the slices with either the selective CCK-2 receptor antagonist CR2945 (3 µ m ), or 6,7-dinitroquinoxaline-2,3(1H,4H)-dione (DNQX), 10 µ m , a glutamatergic (+/–)-α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptor antagonist. It is suggested that CCK modulates glutamate-GABA mechanisms by acting on CCK-2 receptors via volume transmission occurring at the level of the basolateral amygdaloid nucleus and/or by synaptic or perisynaptic volume transmission in the region of the rostrolateral main and paracapsular intercalated islands, resulting in subsequent disinhibition of the central amygdaloid nucleus and anxiety or panic-like behaviour.