白子草总黄酮及总多糖降血糖有效部位的提取工艺研究

目的 研究建立白子草总黄酮及总多糖降血糖有效部位的提取工艺。方法 在单因素试验的基础上,考察提取次数、药材粒径、浸泡时间、料/液比、乙醇浓度、提取时间对白子草总黄酮提取率的影响,并通过L₉（3）⁴正交试验优化总黄酮最佳提取工艺;以前期研究为基础,结合L₉（3）⁴正交试验,优化总多糖最佳提取工艺。结果 白子草总黄酮最佳提取工艺为：药材最粗粉加20倍80%乙醇,浸泡0.5 h,回流提取2次,每次1.0 h;总多糖最佳提取工艺为：醇提后药渣加20倍纯净水,80℃回流提取2次,每次1.0 h。该条件下白子草总黄酮及总多糖提取率均大于80%。结论 本研究建立的白子草总黄酮及总多糖降血糖有效部位提取工艺稳定、重复性好,为白子草降血糖活性研究奠定了实验基础。     

正交试验优选复方金沙利胆颗粒的提取工艺

摘 要 目的：研究探讨复方金沙利胆颗粒的最佳提取工艺条件。方法: 根据处方中药所含主要成分的性质,通过正交试验对提取条件进行了筛选优化。以芍药苷含量和浸膏得率作为考察评价指标,选择加水量,煎煮时间,煎煮次数作为考察的三个影响因素进行优选。每因素设置3个水平,以L₉(3⁴ )正交表进行正交试验。结果: 通过正交试验确定了复方金沙利胆颗粒的最佳工艺为加12倍水（第一次提取加14倍水,浸泡30 min）,提取2次,每次煎煮1 h。结论:该工艺提取率高,稳定性好,操作简单,浸膏得率较高,质量可控,值得推广应用。     

正交试验法优选金铃子颗粒提取工艺

摘 要 目的：：优选金铃子颗粒的提取工艺。 方法: 用正交试验法考察加水量、煎煮时间、煎煮次数等因素对提取工艺的影响,以干浸膏得率和延胡索乙素含量为考察指标,烘干法测定干浸膏得率,高效液相色谱法测定延胡索乙素含量。 结果: 加10倍量水,煎煮1 h,煎煮 3 次为最佳提取工艺。 结论: 优选的工艺合理可行、重复性良好、提取效率高,适合于工业化生产。     

正交试验法优选葛花异黄酮的提取工艺

目的 优选葛花异黄酮的提取工艺。 方法 乙醇回流提取葛花异黄酮,采用紫外分光光度(UV)法和高效液相色谱(HPLC)法测定葛花中总黄酮及鸢尾苷、鸢尾苷元含量。在对乙醇浓度、溶剂用量、提取时间等进行单因素考察基础上,选用L₉(3⁴)正交设计试验优选提取工艺。 结果 葛花异黄酮的最佳提取工艺为第1次加入12倍量70%乙醇提取90 min,第2次加入10倍量70%乙醇提取60 min。 结论 优选的葛花异黄酮提取工艺合理可行,能为实际生产提供参考。     

多目标遗传算法优化金荞麦的提取工艺

目的 优选金荞麦的提取工艺。方法 选择乙醇浓度、溶媒倍数、提取时间、提取次数为考察因素,以总黄酮和浸膏得率为考察指标进行正交试验,运用SPSS 19.0软件建立总黄酮和浸膏得率的二次回归模型,采用多目标遗传算法对其进一步优化,确定金荞麦的最优提取工艺。结果 金荞麦的最佳提取条件：加金荞麦药材24倍量的61%乙醇于80℃提取3次,每次1.90 h;总黄酮和浸膏得率分别为11.58%和22.83%,与遗传算法模型预测结果相符。结论 多目标遗传算法优化的效果理想,所得工艺稳定可行,有效成分得率高,可用于金荞麦有效部位的提取。     

Box-Behnken设计响应面法优选水杨梅总黄酮提取工艺研究

摘 要 目的： 采用Box Behnken设计响应面法优化水杨梅的最佳提取工艺。方法: 以水杨梅中总黄酮含量为评价指标,通过单因素试验分别考察乙醇浓度、液料比、提取时间三个因素对总黄酮含量的影响,采用Box Behnken设计响应面法对水杨梅的提取工艺参数进行优化。结果: 水杨梅的最佳提取工艺：乙醇浓度为 50%,液料比为4.2倍,提取时间为80 min,在该条件下平均提取量12.590 0 mg·g^-1。结论:Box Behnken设计响应面法优化水杨梅总黄酮提取工艺合理,建立的数学模型和试验数据相符,具有较好的预测性。     

响应面法优化雪松松针中金丝桃苷的回流提取工艺

目的 优化雪松松针中金丝桃苷的回流提取工艺。方法 采用HPLC测定雪松松针中金丝桃苷的含量;基于单因素试验结果,以金丝桃苷含量为指标,根据Box-Behnken设计对影响回流提取的3个因素（料液比、乙醇浓度、提取时间）进行考察;通过响应面分析优化雪松松针中金丝桃苷的最佳回流提取工艺。结果 优化得到的最佳回流提取工艺参数为乙醇浓度60%、料液比1︰16（g·mL^-1）、回流提取1次,时间为100 min;在此工艺条件下提取得到的金丝桃苷平均含量为0.119 6 mg·g^-1,与预测值0.119 4 mg·g^-1的相对偏差较小。结论 优选得到的雪松松针中金丝桃苷回流提取工艺合理、可行。     

恩施巴戟环烯醚萜苷类成分提取工艺优选及抗氧化活性研究

目的 优化恩施巴戟中主要环烯醚萜苷类成分提取工艺,评价恩施巴戟体外抗氧化活性。方法 选择经典的加热回流提取法,以乙醇体积分数、溶剂倍量、提取时间为考察因素,以浸膏得率和水晶兰苷含量的综合评分为评判指标,设计正交试验筛选最佳提取工艺条件;测定总还原能力、DPPH清除率、羟自由基清除率,检测其体外抗氧化活性。结果 最佳提取工艺条件为6倍量的60%的乙醇加热回流2 h;恩施巴戟具有一定的抗氧化能力,乙酸乙酯部位活性最佳。结论 优化的提取工艺稳定可行,可用于提取恩施巴戟的环烯醚萜苷类成分,该研究初步证明了恩施巴戟具有一定的抗氧化活性。     

响应面法优化胡柚幼果中柚皮苷与新橙皮苷的提取工艺

目的 优选胡柚幼果中柚皮苷与新橙皮苷的提取工艺。方法 在单因素试验的基础上,对乙醇浓度、料液比、提取时间3个因素进行响应面Box-Behnken中心组合设计优化,得到最佳提取工艺。结果 最佳提取工艺条件为乙醇浓度60%、料液比1：10、提取时间1.8 h、回流提取2次,在此条件下柚皮苷与新橙皮苷的总得率为23.44%。结论 本提取工艺方法简单、合理、稳定,为工业化生产提供了一定的依据。     

均匀设计法优选姜石肠炎康颗粒半仿生法提取的工艺条件

摘 要 目的： 优选姜石肠炎康颗粒的半仿生提取条件。方法: 采用均匀设计法,在处方组成和用量,提取温度,过滤方法、离心时间、浓缩倍数等条件相同的情况下,用不同的pH的水溶液提取方药,以煎煮用水的pH、煎煮用水量和提取时间为考察因素,以盐酸小檗碱、秦皮甲素、乙醇浸出物和干浸膏的含量为评价指标,数据经标准化处理后,综合评价,优选其最佳的提取工艺。结果: 最佳提取条件为：2次煎煮用水的pH分别为2.013和7.004;用水量为药材质量的12倍;2次提取时间分别为2 h和1.999 9 h。结论: 优选出的半仿生法提取姜石肠炎康颗粒工艺条件合理,稳定,可行。可用于本院内制剂的生产。     

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.     

Nachweis einiger Heilmittel in der Kniegelenksynovialflüssigkeit

Zusammenfassung Mittels Gaschromatographie und Dünschichtchromatographie wiesen die Autoren 11 Substanzen nach, welche durch Injektion oder nach Verabreichung per os in die Kniegelenksynovialflüssigkeit eindrangen. In ihrer Aufstellung konnten sie eine direkte Beziehung zwischen Struktur sowie chemischphysikalischen Eigenschaften der Substanz und ihrer Fähigkeit, aus dem Blut in die Kniegelenksynovialflüssigkeit einzudringen, nicht nachweisen, außer der Tatsache, daß Substanzen mit starker Affinität zu Eiweißstoffen erst in höheren Dosen nachweisbar waren.     

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.