近红外光谱法在药学上的应用

介绍了近红外光谱法的基本原理,及其在药物原材料,包装材料,制剂分析,生产过程监控及质量控制等方面的应用。     

脑室灌注β-淀粉样肽致痴呆动物模型

目的　建立脑室灌注 β 淀粉样肽 (Aβ)致痴呆动物模型及观测指标。方法　微泵渗透对动物脑室进行灌注可溶性大片段Aβ ,侧脑室一次性注射聚集态小片段Aβ,侧脑室一次性注射可溶性大片段Aβ片段 ,侧脑室注射Aβ联用转化生长因子β(TGFβ)。 结果　上述方法处理后动物水迷宫和被动回避操作能力受损 ,学习和记忆功能损害 ,皮层和海马中胆碱乙酰转移酶 (ChAT)活性明显降低 ,抗氧化能力下降 ,海马神经元坏死或缺失 ,凋亡相关蛋白酶Bal 2、Bax和p5 3增加等。结论　上述方法均可选用来作为模拟AD病理特征的动物模型。     

Enhancing the Buccal Mucosal Delivery of Peptide and Protein Therapeutics

Pharmaceutical Research - With continuing advances in biotechnology and genetic engineering, there has been a dramatic increase in the availability of new biomacromolecules, such as peptides and...     

康欣胶囊及其拆方对血管性痴呆肾虚血瘀型模型大鼠外周血CD3、CD4、CD8和CD4/CD8的影响

目的 　观察康欣胶囊及其拆方对 ( VD)模型 (肾虚血瘀型 )大鼠外周血 CD3、CD4、CD8的影响。 方法 　采用电灼烧封闭双侧椎动脉和摘除单侧性器官法制作 ( VD)模型 (肾虚血瘀型 )大鼠 ,用康欣胶囊全方及其拆方和西药喜得镇给药 1个月 ,电镜、光镜观察各组大鼠海马、下丘脑、枕部皮质神经细胞情况 ,流式细胞仪检测大鼠外周血 CD3、CD4、CD8。 结果 　康欣胶囊全方组海马、下丘脑、枕部皮质神经细胞的内织网、线粒体水肿固缩及细胞核固缩情况明显轻于模型空白对照组 ;外周血 CD4/ CD8比例指标明显高子空白模型组、健脾组、西药组 ( P<0 .0 1) ,养血活血组 CD4/ CD8比例指标高于空白模型组、健脾组 ( P<0 .0 5 )。结论 　康欣胶囊全方及其拆方养血活血方可提高 ( VD)模型 (肾虚血瘀型 )大鼠外周血 CD4/ CD8比例水平即提高免疫力 ,并延缓减轻缺血性神经细胞凋亡。     

泼尼松龙葡聚糖前体药物的结肠定位转释机制研究

目的　探讨泼尼松龙葡聚糖前体药物的结肠定位释放机制。方法　将前体药物分别与不同pH值缓冲液、含葡聚糖酶的缓冲液及含大肠杆菌的培养基于 37℃水浴中一起孵育 ,采用HPLC法测定前体药物释放泼尼松龙的情况。结果　前体药物在接近胃肠道下部pH值的缓冲液中 ,活性药物释放量多 ;葡聚糖酶及大肠杆菌均能明显促进活性药物的释放。结论　泼尼松龙葡聚糖前体药物的结肠定位转释作用可能是前体药物到达结肠时 ,在其特殊 pH环境、微生物及其分泌的酶的共同作用下释放出活性药物     

长链非编码RNA与乳腺癌侵袭转移相关性研究进展

摘要： 长链非编码 RNA（lncRNA）是一类长度大于 200 nt, 不具备编码蛋白质能力的功能性 RNA 分子。研究发现, lncRNA 的异常表达与乳腺癌的进展关系密切, 部分 lncRNA 参与调控乳腺癌侵袭转移的过程。本文对乳腺癌中异常表达的 lncRNA 及其与乳腺癌侵袭转移的相关性进行综述, 以期为乳腺癌的诊疗提供新的思路。     

超高效液相串联质谱法同时测定保健食品中10种水溶性维生素

目的：建立超高效液相色谱-串联质谱检测方法同时测定保健食品中10种水溶性维生素。方法：样品经过前处理后,采用Waters ACQUITY UPLC HSS T3（2.1×100 mm,1.8μm）色谱柱分离;以0.1%甲酸的甲醇溶液和0.1%甲酸的水溶液为流动相进行梯度洗脱,通过电喷雾离子源多反应监测（MRM）模式进行检测。结果：10种水溶性维生素在6 min内完成分离,线性关系良好（r≥0.997）,方法检出限在5~250μg·kg^-1之间。3个添加水平的回收率和相对标准偏差RSD（n=6）分别为85.9%~109.5%和1.09%~0.79%。结论：该方法简便、快速、准确、灵敏,适用于保健食品中水溶性维生素的测定。     

青霉素超敏反应及其诊断技术研究进展

介绍了青霉素的化学结构、抗原决定簇、过敏原的产生、超敏反应的特点以及交叉过敏情况,并对常见的诊断技术（皮试）和体外诊断新方法进行了介绍和比较.     

Tanshinone IIA triggers p53 responses and apoptosis by RNA polymerase II upon DNA minor groove binding

Our previous work has shown that tanshinone IIA (Tan IIA) is a DNA minor groove binder instead of an intercalator as previously thought. In this study, we have further demonstrated that the molecular antitumor pharmacology of Tan IIA is dependent on its groove-binding capability. First, we investigated the structure damage to duplex DNA upon Tan IIA binding using circular dichroism spectra. Subsequently, we performed western blot, flow cytometry analysis, chromatin immunoprecipitation, and quantitative real-time PCR to illustrate the RNAPII degradation, phosphorylation, and distribution along the transcribed gene in H22 cells exposed to Tan IIA. In addition, p53 activation and apoptosis induction in both cultured H22 cells and in mice bearing the ascitic-type H22 were measured following Tan IIA treatment. It was revealed that Tan IIA decreases the level of RNAPII by altering DNA structure. At the low dose range (0.2-4 μM) of Tan IIA exposure, the DNA structure damage results in the inhibition of RNAPII binding to DNA and the initiation of RNAPII phosphorylation, while higher concentrations of Tan IIA (4-20 μM) cause complete phosphorylation and degradation of RNAPII followed by p53 activation and apoptosis. A similar apoptosis induction by RNAPII was observed in animals. Apoptosis of tumor cells from ascitic fluid was not detected until RNAPII levels were downregulated by Tan IIA, which requires 40 mg/kg body weight of Tan IIA. It was concluded that DNA-conformational-damage-dependent RNAPII response upon groove binding is the molecular basis of the antitumor property of Tan IIA, in vivo and in vitro.