跌打活血涂膜剂质量控制研究

目的 :建立跌打活血涂膜剂质控方法。方法 :采用薄层鉴别法对跌打活血涂膜剂进行定性 ,并采用分光光度法在512nm波长处测定该药中大黄素的含量。结果 :平均回收率为101.2 % ,精密度为0.78 %。结论 :该方法重现性好 ,可作为本品的质量控制标准     

促进剂对跌打活血涂膜剂经皮渗透的影响

目的建立跌打活血涂膜剂体外经皮渗透检测方法,考察促进剂对跌打活血涂膜剂经皮渗透的影响。方法以双室渗透扩散装置进行体外渗透实验,采用紫外分光光度法测定和计算药物的积累渗透百分率（Q）,筛选促进剂。结果在几种曲型促进剂中,对涂膜剂的促渗作用依次为月桂氮卓酮、丙二醇、油酸。月桂氮卓酮阻碍涂膜剂中作用的最佳浓度为体积分数的2%。结论采用紫外分光光度法检测涂膜剂的累计渗透百分率,无需分离成分。跌打活血涂膜剂中选择体积分数为2%的月桂氮卓酮为促进剂,可使涂膜剂的渗透率提高     

薄层扫描法测定降粘活血饮中大黄素的含量

目的 :研究测定降粘活血饮中大黄素含量的方法。方法 :采用薄层扫描法对降粘活血饮中有效成分大黄素进行含量测定。结果 :测得每克降粘活血饮粉末中的大黄素平均含量为 0 .70mg。 结论 :该法快速简便 ,准确可靠 ,可作为降粘活血饮质量控制指标     

用均匀设计法优选跌打活血涂膜剂的提取工艺

目的：优选简便可靠的提取工艺。方法：用均匀设计法对跌打活血涂膜剂的提取工艺中乙醇浓度、回流时间、回流次数、乙醇用量、药材粒度５个因素进行优选;用紫外分光光度法测定提取液的吸收度值作为评价指标。结果：在跌打活血涂膜剂的提取工艺中采用浓度９５％乙醇,回流时间 １ｈ,回流次数４次,乙醇用量 １０倍,药材粒度 ０．２ｍｍ为最佳工艺。结论：本文建立的提取工艺方法简便、可靠。     

桃核承气缓释片的稳定性研究

目的:考察桃核承气缓释片的稳定性,预测其有效期;了解影响其稳定性的因素,为加速试验和长期试验提供依据。方法:通过经典恒温加速试验和影响因素试验法考察稳定性,采用高效液相色谱法测定制剂中大黄酸和大黄素的含量。结果:大黄酸的有效期为2.42年,大黄素的有效期为2.40年;强光照射对桃核承气缓释片的稳定性有一定影响,高温和高湿度对其稳定性影响很小。结论:桃核承气缓释片室温下的有效期为2年。为了有利于制剂的质量、安全性和有效性,生产和贮藏过程中应采用适当的避光措施。     

酮康唑涂膜剂热稳定性研究

采用反相高效液相色谱法测定酮康唑涂膜剂中的酮康唑含量,用加温加速实验法研究该涂膜剂的热稳定性动力学。结果表明其降解反应为一级动力学过程,预测其半衰期和有效期分别为11.4年和1.7年。     

烧伤涂膜剂质量标准研究

目的建立烧伤涂膜剂的质量控制方法。方法用薄层色谱法(TLC法)鉴定涂膜剂中的虎杖、黄芩,用高效液相色谱法(H PLC法)测定虎杖中大黄素含量。结果TLC法鉴定结果满意;回归方程为A=3.18×107C+2.03×105(r=0.9997),大黄素浓度在0.1～0.5m g m/L范围内与峰面积线性关系良好,平均加样回收率为98.67%(n=6)。结论该法操作简便,结果可靠,重现性好,可作为烧伤涂膜剂的质量控制方法。     

伤速康涂膜剂的质量标准研究

目的建立伤速康涂膜剂的质量标准。方法采用TLC法对处方中大黄、栀子进行定性鉴别，并采用反相高效液相色谱法对涂膜剂中的大黄素、绿原酸进行含量测定。结果大黄素的平均回收率为101．8％，RSD为1．96％，绿原酸的平均回收率为102．1％，RSD为2．0％。结论该方法简便易行，重现性好，可作为本品的质量控制标准。     

正交试验优选疗筋涂膜剂醇提工艺

目的:优选疗筋涂膜剂的醇提工艺。方法:以醇浸膏得率和大黄素含量为考察指标,采用正交试验法,考查乙醇浓度、加醇量及提取时间对提取工艺的影响。结果:最佳醇提工艺为A2B2C2,即药材加6倍量70%乙醇提取2次,第1次提取1.5h,第2次提取1h。结论:优选的疗筋涂膜剂的醇提工艺简便、快速、准确,可为工业化生产提供理论依据。     

烫伤膜的制备

目的:建立烫伤膜剂的制备工艺与质量评价.方法:用脱乙酰甲壳素作为基质,利用醇提法提取,制成涂膜剂;采用HPLC测定大黄素的含量.结果:制备的涂膜剂质地均匀细腻,涂展性好,刺激性小,释放药物快,含量测定简单易行.结论:该涂膜剂配方合理,符合中国药典2000年版的规定,可作为新制剂用于临床.     

跌打活血酊药效学实验研究

目的:研究跌打活血酊药效学.方法:采用实验性大鼠足跖肿胀、肉芽肿和小鼠腹腔血管通透性实验.结果:跌打活血酊非常显著促进小鼠瘀血吸收、消散作用,而对小鼠热板性致痛及化学性致痛均无显著性镇痛作用.结论:跌打活血酊具有明显的抗炎作用.     

Alaternin and emodin with hydroxyl radical inhibitory and/or scavenging activities and hepatoprotective activity on tacrine-induced cytotoxicity in HepG2 cells

The antioxidative and hepatoprotective potentials of two anthraquinones, alaternin (2-hydroxyemodin) and emodin, to scavenge and/or inhibit hydroxyl radicals generated by the Fenton reaction and to protect tacrine-induced cytotoxicity in human liver derived HepG2 cells were evaluated, respectively. The inhibitory activity on hydroxyl radical generated in a cell-free chemical system (FeSO4/H2O2) was investigated by a fluorescence spectrophotometer using a highly fluorescent probe, 2',7'-dichlorofluorescein. The hydroxyl radical scavenging activity was determined by electron spin resonance spectroscopy using 5,5-dimethy-1-pyrroline-N-oxide as hydroxyl radicals trapping agents. Tacrine-induced HepG2 cell toxicity was determined by a 3-[4,5-dimethylthiazole-2yl]-2,5-diphenyltertrazolium bromide assay. Although the scavenging activity of alaternin on hydroxyl radical was similar to that of emodin in dose-dependent patterns, the inhibitory activity exhibited by the former on hydroxyl radical generation was stronger than that of the latter, with IC50 values of 3.05 +/- 0.26 microM and 13.29 +/- 3.20 microM, respectively. In addition, the two anthraquinones, alaternin and emodin showed their hepatoprotective activities on tacrine-induced cytotoxicity, and the EC50 values were 4.02 microM and 2.37 microM, respectively. Silymarin, an antihepatotoxic agent used as a positive control exhibited the EC50 value of 2.00 microM. These results demonstrated that both alaternin and emodin had the simultaneous antioxidant and hepatoprotective activities.     

如意金黄散膜剂的制备

目的以脱乙酰壳聚糖为成膜材料制备了如意金黄散膜剂。方法兼顾如意金黄散中各主要成分的溶解性，以乙醇为溶剂提取有效成分，以壳聚糖为成膜材料制备膜剂，HPLC测定膜剂中的姜黄素、大黄酸、大黄素、大黄酚、小檗碱的含量。结果以膜剂中大黄酸的释放度为评价指标，膜剂体外缓释效果良好。结论以壳聚糖为成膜材料制备如意金黄散膜剂柔性良好，大黄酸体外缓释作用良好。     

薄层扫描法测定复方甘黄胶囊中大黄素的含量

目的:考查复方甘黄胶囊中大黄素含量的测定方法。方法:采用薄层扫描法对复方甘黄胶囊中有效成分大黄素进行含量测定。结果:复方甘黄胶囊中大黄素平均含量为0.19 mg/g。结论:方法准确可靠,可作为复方甘黄胶囊质量控制指标。     

不同浓度甲醇对决明子中5种蒽醌类成分含量的影响考察

目的:考察不同浓度甲醇对决明子中5种蒽醌类成分含量的影响。方法:用不同浓度(95%、80%、30%)甲醇溶液提取决明子药材,采用高效液相色谱法测定药材中芦荟大黄素、大黄酸、大黄素、大黄酚、大黄素甲醚的含量。结果:不同浓度甲醇溶液提取的决明子药材中芦荟大黄素、大黄酸、大黄素、大黄酚、大黄素甲醚的含量范围分别为0.0010～0.0181、0.0104～0.0637、0.0209～0.2535、0.0031～0.9157、0.0051～0.1263mg·g-1;平均回收率范围为96.34%～97.16%,RSD均小于3%(n=5)。结论:不同浓度甲醇提取的决明子药材中5种蒽醌类化合物含量差异大;以95%甲醇提取效果最佳,30%甲醇提取效果最差。     

Silk fibroin mediated delivery of liposomal emodin to breast cancer cells

The efficacy of a drug is dependent on its mode of delivery and its potency at the tumor site. In this study, the drug delivery and efficacy of silk fibroin coated liposomes (SF-ELP), encapsulating a receptor tyrosine kinase inhibitor, emodin, on Her2/neu over-expressing breast cancer cells, was investigated. This study demonstrates that SF-ELP was more efficacious in suppressing the growth of Her2/neu over-expressing breast cancer cells MDA-MB-453 and BT-474 as compared to uncoated emodin loaded liposomes (ELP). Reduced levels of phosphorylated Her2/neu correlated with growth inhibition observed in the MDA-MB-453 cells, treated with both ELP and SF-ELP. ELP treatment of MDA-MB-453 breast cancer cells resulted in inhibition of the PI3K pathway whereas SF-ELP treatment inhibited both the PI3K and MAPK pathways, which contributed to the enhanced growth inhibitory effects of Her2/neu over-expressing breast cancer cells. Coating of ELP with silk fibroin did not alter the target specificity of emodin, on the other hand the emodin efficacy was enhanced. Higher uptake of emodin delivered by SF-ELP lead to increased cell death as compared to emodin delivery via ELP. Silk fibroin coating around the liposome imparts an extra layer that emodin has to extravasate in order to release from the encapsulating liposome. This increases retention of the drug in the cell for a longer time and protects emodin from quick release and metabolism. Longer intracellular retention may lead to the longer availability of emodin for down-modulation of various Her2/neu pathways. This study demonstrates that silk fibroin coating enhanced emodin delivery in Her2/neu over-expressing breast cancer cells thereby increasing the overall efficacy of the drug.