分光光度法测定维吾尔药昆仑雪菊中总皂苷的含量

目的研究维吾尔药昆仑雪菊总皂苷的含量测定方法。方法用乙醇提取,水饱和正丁醇萃取提取纯化昆仑雪菊中的总皂苷;高氯酸显色,紫外分光光度法测定总皂苷的含量。结果以人参皂苷Rb1作标准曲线,A=0.0666C-0.0048,r=0.9997,样品质量浓度在4.5～10.5μg.mL-1范围内与吸光度线性关系良好,回收率为103.82%,昆仑雪菊总皂苷的含量为8.36%。结论该方法简便、快速、灵敏、准确,可作为维吾尔药昆仑雪菊中总皂苷的含量测定方法。     

三七中总皂苷的含量测定

目的测定三七的不同溶剂浸提液中总皂苷的含量。方法采用标准曲线法。结果无水甲醇是浸提三七中皂苷类化合物的较理想溶剂,以三七皂苷R1为标准品测得该提取液中总皂苷含量为12.3%。结论该方法简便,可作为三七中皂苷类物质的含量测定方法。     

不同产地延龄草中延龄草总皂苷的含量测定

目的建立延龄草中总皂苷的含量测定方法,比较研究不同产地延龄草中总皂苷的含量。方法以薯蓣皂苷元为对照品,采用分光光度法,高氯酸显色,在410nm处测定吸光度,计算延龄草中总皂苷的含量。结果薯蓣皂苷元在4.12~49.44μg范围内与吸光度值呈良好的线性关系(r=0.998 9),平均回收率为97.3%,RSD为2.5%。结论该方法操作简便、准确、灵敏、重复性好,可用于延龄草样品中总皂苷的含量测定,不同产地样品,总皂苷含量有差异。     

荨麻总皂苷的提取纯化和含量测定

目的:本文是论述测定广西荨麻中总皂苷的含量的方法。方法:以胡萝卜苷为标准对照品,5%香草醛-冰醋酸、高氯酸为显色剂,采用紫外分光光度法,在542nm处测定吸光度,计算荨麻中总皂苷的含量。结果:荨麻的总皂苷浓度在0.0018-0.0072mg/ml与吸光度呈良好的线性关系Y=11.528X+0.117(r=0.9988),平均回收率为98.69%(n=6),RSD=1.11%;荨麻中总皂苷的含量为21.3mg/g。并建立了荨麻中总皂苷超声提取的提取方法和紫外-可见分光光度法对其含量测定方法。结论:此方法方便,准确性高,稳定性好,可用于荨麻药材的总皂苷的含量测定。     

HPLC法测定远志中总皂苷的含量

目的:建立远志药材中总皂苷的含量测定方法。方法:采用远志提取物碱水解方法制备远志总皂苷的次级苷—细叶远志皂苷,采用高效液相色谱法测定细叶远志皂苷的含量。色谱条件为 Alltima C_(18)色谱柱(4.6 mm×250 mm,5 μm),流动相为甲醇0.05%磷酸溶液(65:35),流速1.0 mL·min~(-1),检测波长202 nm。结果:细叶远志皂苷的理论塔板数为2500。回归方程 Y=4.242×10~6X-1.068×10~4(r=0.9999),线性范围100～1000μg·mL~(-1)。平均回收率(n=6)为101.2%(RSD=3.6%)。不同来源14批远志药材含量测定结果表明,远志中含总皂苷以细叶远志皂苷计为2.42%～3.71%;不同采收期样品分析表明,以3～6月份采收含量较高;1～3年生样品分析表明,以2年生和3年生药材含量为高。结论:该方法简便、准确,重复性好,可作为远志药材及含远志复方制剂质量控制方法。建议远志含总皂苷以细叶远志皂苷计应不低于2.5%,采收时间以春季为佳,生长期以2年以上为佳。     

NIRS结合PLS算法快速测定西洋参饮片中人参皂苷Rg_1、Re、Rb_1的总含量

目的:建立快速测定西洋参饮片中人参皂苷Rg_1、Re、Rb_1总含量的方法。方法:采用高效液相色谱法测定饮片中人参皂苷Rg_1、Re、Rb_1的总含量(作为参考值)。采用红外漫反射光谱技术(NIRS)结合偏最小二乘法(PLS)建立饮片中人参皂苷Rg_1、Re、Rb_1总定量模型:根据参考值采集62份饮片样品,以标准归一化法联合一阶导数法预处理光谱,饮片样品中人参皂苷Rg_1、Re、Rb_1总含量测定最佳波段为7 664.23~5 236.05 cm~(-1)。结果:饮片样品中人参皂苷Rg_1、Re、Rb_1总含量测定方法学验证符合要求。人参皂苷Rg_1、Re、Rb_1总定量模型的校正集相关系数为0.991 03,校正均方差为0.010 26。结论:该方法快速准确、简便无污染,可用于西洋参饮片中人参皂苷Rg_1、Re、Rb_1总含量的快速测定。     

紫外分光光度法测定吉祥草中的总皂苷

目的 建立测定吉祥草中总皂苷含量的方法,并测定不同来源的吉祥草药材中总皂苷的含量.方法 采用UV法,在453nm处测定吉祥草中总皂苷的含量.结果 凯提皂苷元26-136μg与吸光度的线性关系良好(r=0.9996),方法的平均回收率为97.3%(n=9),RSD=1.8%;不同来源的吉祥草药材中总皂苷含量有较大差异.结论 所用测定方法简便、准确、灵敏、可靠,可控制吉祥草的药材质量.     

补肾活血方中人参总皂苷含量测定

目的:建立补肾活血方中人参总皂苷含量测定方法。方法:以人参皂苷Re为对照品,香草醛-高氯酸显色,采用分光光度法于544 nm处测定补肾活血方中人参总皂苷的含量。结果:在50.1~150.3μg范围内,对照品Re的吸光度与含量线性关系良好(r=0.9996),平均回收率为99.95%,RSD=2.33%(n=6)。结论:该法精密度、重现性良好,可作为补肾活血方人参总皂苷的含量测定方法。     

柴胡中柴胡总皂苷及柴胡皂苷a的含量测定

目的 建立柴胡中柴胡总皂苷及柴胡皂苷a的含量测定方法,并对样品进行含量测定.方法 采用紫外分光光度法,以柴胡皂苷a为对照品,在波长545nm处对样品中的总皂苷进行含量测定;采用高效液相色谱法,以C18色谱柱(4.6mmX250mm.5μm)、甲醇-水为流动相,流速为1mL·min<'-1>,检测波长为210nm,测定样品中柴胡皂苷a的含量.结果 柴胡总皂苷在30～70μg/mL、柴胡皂苷a在50.4～252μg/mL范围内呈良好的线性关系,r分别为09956、0.9991;平均回收率:柴胡总皂苷为99.31%、柴胡皂苷a为99.22%;RSD:柴胡总皂苷为1.25%,柴胡皂苷a为1.07%.结论 本研究所建立的紫外分光光度法测定柴胡总皂苷及高效液相法测定皂苷a含量的方法,简便、易行、快速,结果准确可靠,适用于柴胡中柴胡总皂苷及柴胡皂苷a的含量测定,并为在安全剂量范围内正确使用柴胡提供依据.     

不同提取方法对土牛膝总皂苷含量测定的影响

目的建立土牛膝中总皂苷的含量测定方法,并考察不同提取方法对土牛膝中总皂苷含量测定的影响。方法采用比色法测定总皂苷的含量,分别考察甲醇回流提取、乙醇回流提取等5种提取方法制得的样品溶液所测定的总皂苷的含量。结果甲醇回流提取、乙醇回流提取、水超声提取、乙醇超声提取及索氏回流提取制备的样品溶液中总皂苷的含量分别为3.36%,4.75%,2.63%,4.97%,2.14%。结论比色法可用于土牛膝总皂苷含量测定,样品溶液的制备宜采用乙醇超声提取法。     

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.