泽兰及泽桂癃爽胶囊中熊果酸的HPLC测定

建立了高效液相色谱法测定泽兰药材及泽桂癃爽胶囊中熊果酸的含量.采用ODS C18柱,甲醇-水-乙酸-三乙胺(87:13:0.04:0.02)为流动相,检测波长215nm.熊果酸在2.5×10-4～4×10-3mg范围内线性关系良好.泽兰药材中熊果酸平均回收率为98.0%(RSD 1.47%),泽桂癃爽胶囊中熊果酸回收率为97.3%(RSD 1.63%).     

用HPLC法测定泽桂隆爽胶囊中肉桂酸的含量

目的:建立用HPLC法测定泽桂隆爽胶囊中肉桂酸含量的方法。方法:采用Shim-pack ODS色谱柱(250 mm×4.6 mm,5μm),流动相为甲醇-乙腈-水-冰醋酸(10∶22∶55∶0.5),用前经0.45μm膜过滤;流速1.0 ml/min;检测波长272 nm。结果:肉桂酸的线性范围为1.6~8μg/ml,r=0.999 5,平均加样回收率为98.36%,RSD为0.56%(n=5)。结论:本方法精密度高,分离度好,可用于泽桂隆爽胶囊中肉桂酸的含量测定。     

高效液相色谱法测定泽虎降脂胶囊中大黄素含量

目的建立测定泽虎降脂胶囊中大黄素含量的高效液相色谱法。方法色谱柱为Alltima C18柱(250 mm×4.6 mm,5μm),流动相为甲醇-0.1%磷酸溶液(85∶15),流速为1.0mL/min,检测波长为287nm,柱温为30℃。结果大黄素进样量在0.0890～0.8900μg范围内与峰面积线性关系良好,r=0.9999(n=5);平均加样回收率为98.04%,RSD为1.91%(n=6)。结论该方法简便、准确、重现性好,可用于泽虎降脂胶囊的含量测定。     

高效液相色谱法测定九味肝泰胶囊中姜黄素含量

目的建立九味肝泰胶囊中姜黄素的含量测定方法。方法采用Zorbax SB-C18柱(250 mm×4.6 mm,5μm),流动相为乙腈-0.2%磷酸溶液(50∶50),检测波长为430 nm,柱温为35℃。结果姜黄素进样量在0.004 0～0.099 2μg范围内与峰面积呈良好的线性关系(r=0.999 9),平均回收率为97.38%,RSD=0.50%(n=6)。结论该方法操作简便、准确、专属性强、重现性好,可用于九味肝泰胶囊中姜黄素的含量测定。     

HPLC法测定地泽胶囊中齐墩果酸的含量

目的建立HPLC法测定地泽胶囊中齐墩果酸的含量。方法采用HPLC法,色谱柱为Hypersil ODS C18（4.6×250mm,5μm）,检测波长为215nm,流动相为乙腈-水-醋酸铵（79∶20∶0.8）,流速为1.0mL.min^-1。结果齐墩果酸在浓度0.486～2.43μg范围内线性关系良好（r=0.9997）,平均回收率为100.5%,RSD为0.3%。结论本方法操作简便,快速,重复性好,精密度高,结果准确可靠,可用于地泽胶囊中齐墩果酸的含量测定。     

二阶导数紫外光谱法测定双黄连口服液中总绿原酸的含量

目的 建立二阶导数光谱法测定双黄连口服液中总绿原酸含量的方法.方法 用二阶导数光谱法直接测定双黄连口服液中总绿原酸含量,于357.9 nm波长处测定振幅D值.结果 绿原酸在4.67～23.35 mg·L-1范围呈良好线性关系;其回归方程为D=0.7495×10-4C-0.1×10-4(r=0.9972);平均回收率102.56%、RSD=2.09%(n=5),24 h内D值无明显变化,RSD=3.15%.结论 本方法操作简单、准确,可用于测定双黄连口服液中总绿原酸含量.     

RP-HPLC测定参仁强体胶囊中橙皮苷的含量

目的 测定参仁强体胶囊中橙皮苷的含量.方法 采用RP-HPLC法,用Aichrom Bond-AQ C18柱(250 mm×4.6mm,5 μm,),以甲醇-醋酸-水(35:4:61)为流动相,流速1.0ml·min-1,检测波长283 nm.结果 在0.074～1.107 μg范围内与峰面积呈很好的线性关系,回归方程为:Y=1.000 ×106X 2.155×104(r=0.9994),平均回收率为99.4%(RSD=0.27%,n=5).3批样品中橙皮苷的平均含量分别为每粒1.35、1.38、1.41 mg(n=2).结论 所建方法简便、准确、重复性好,可用于参仁强体胶囊中橙皮苷的含量测定.     

HPLC测定西咪替丁胶囊的含量

目的 建立西咪替丁胶囊的含量测定方法.方法 采用Waters高效液相色谱仪,TIANHE C18柱 (250 mm ×4.6 mm,10 μm),0.05 mol·L-1磷酸二氢钾溶液(三乙胺调节pH至5.8)-甲醇(210:300)为流动相,检测波长为219 nm测定西咪替丁胶囊的含量.结果 使用高效液相色谱法可以准确有效地测定西咪替丁胶囊的含量.结论 该方法在5～50 μg·ml-1的浓度范围内线性关系良好(r=0.9999,n=6),平均回收率为100.3%,RSD=0.6%(n=6),方法简便,准确,适用于西咪替丁胶囊的含量测定.     

HPLC法测定盐酸氟桂利嗪胶囊的含量

目的:建立高效液相色谱法测定盐酸氟桂利嗪胶囊的含量。方法:用C_(18)柱,以乙腈-水(320 mL中加入十二烷基硫酸钠2.0 g和磷酸1.0 mL)(68:32)为流动相,流速为1.0 mL·min~(-1)检测波长为254 nm。结果:盐酸氟桂利嗪在10—90μg·mL~(-1)浓度范围有良好线性关系,r=O.9999,方法回收率为99.6%(n=7),RSD为0.8%。结论:该方法是一种简便、灵敏、准确的分析法,能有效地控制盐酸氟桂利嗪胶囊的质量。     

HPLC测定西咪替丁胶囊的含量

目的建立西咪替丁胶囊的含量测定方法。方法采用W aters高效液相色谱仪,TIANHE C18柱(250 mm×4.6 mm,10μm),0.05 mo.lL-1磷酸二氢钾溶液(三乙胺调节pH至5.8)-甲醇(210∶300)为流动相,检测波长为219 nm测定西咪替丁胶囊的含量。结果使用高效液相色谱法可以准确有效地测定西咪替丁胶囊的含量。结论该方法在5~50μg.m l-1的浓度范围内线性关系良好(r=0.9999,n=6),平均回收率为100.3%,RSD=0.6%(n=6),方法简便,准确,适用于西咪替丁胶囊的含量测定。     

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.     

Efficacy of gut lavage,hemodialysis, and hemoperfusion in the therapy of paraquat or diquat intoxication

Clinical and in vitro investigations were carried out to test the efficacy of gut lavage, hemodialysis, and hemoperfusion in the treatment of poisoning with paraquat or diquat. In a patient suffering from diquat intoxication 130 times more diquat was removed by gut lavage 30 h after ingestion than was removed by complete aspiration of the gastric contents.Determination of in vitro clearances for paraquat and diquat by hemodialysis showed that, at serum concentrations of 1–2 ppm, such as are frequently encountered in poisoning in man, toxicologically relevant quantities of herbicide cannot be removed from the body. At a concentration of 20 ppm, on the other hand, hemodialysis proved to be effective, the clearance being 70 ml/min at a blood flow rate of 100 ml/min. The efficacy of hemoperfusion with coated activated charcoal was on the whole better. Especially at concentrations around 1–2 ppm, the clearance values for hemoperfusion were some 5–7 times higher than those for hemodialysis.In a patient suffering from paraquat poisoning, both hemodialysis as well as hemoperfusion were carried out. The in vitro results could be confirmed: At serum concentrations of paraquat less than 1 ppm no clearance could be obtained by hemodialysis while by hemoperfusion with activated charcoal quite high clearance values were measured and the serum level dropped down to zero.

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Zusammenfassung Klinische Untersuchungen und Laboratoriumsversuche wurden durchgeführt, um die Wirksamkeit von Darmspülung, Hämodialyse und Hämoperfusion bei Paraquat- und Deiquat-Vergiftungen zu prüfen.Bei einem Patienten wurde 30 Std nach Deiquat-Aufnahme durch Darmspülung 130mal mehr Deiquat entfernt als durch vollständige Aspiration des Mageninhaltes. In vitro-Versuche ergaben, daß bei Blutserumkonzentrationen von 1–2 ppm, die bei Vergiftungen oft gemessen werden, durch Hämodialyse keine toxikologisch relevanten Paraquat- oder Deiquat-Mengen entfernt werden können. Dagegen erwies sich die Hämodialyse bei 20 ppm und einer Blutumlaufgeschwindigkeit von 100 ml/min mit einer Clearance von 70 ml/min als wirksam. Die Hämoperfusion mit beschicheter Aktivkohle war in diesen Versuchen aber eindeutig überlegen, denn insbesondere bei Konzentrationen um 1–2 ppm waren die Clearance-Werte 5–7mal höher als bei der Hämodialyse.Die in vitro-Ergebnisse wurden bei einem Patienten mit einer Paraquat-Vergiftung bestätigt: Bei Konzentrationen unter 1 ppm war die Hämodialyse wirkungslos, während durch Hämoperfusion relativ hohe Clearance-Werte erreicht wurden, so daß der Serumspiegel rasch unter die Nachweisgrenze abfiel.

     

In vitro studies on sterically stabilized liposomes (SL) as enzyme carriers in organophosphorus (OP) antagonism

This study describes a new approach for organophosphorous (OP) antidotal treatment by encapsulating an OP hydrolyzing enzyme, OPA anhydrolase (OPAA), within sterically stabilized liposomes. The recombinant OPAA enzyme was derived from Alteromonas strain JD6. It has broad substrate specificity to a wide range of OP compounds: DFP and the nerve agents, soman and sarin. Liposomes encapsulating OPAA (SL)* were made by mechanical dispersion method. Hydrolysis of DFP by (SL)* was measured by following an increase of fluoride ion concentration using a fluoride ion selective electrode. OPAA entrapped in the carrier liposomes rapidly hydrolyze DFP, with the rate of DFP hydrolysis directly proportional to the amount of (SL)* added to the solution. Liposomal carriers containing no enzyme did not hydrolyze DFP. The reaction was linear and the rate of hydrolysis was first order in the substrate. This enzyme carrier system serves as a biodegradable protective environment for the recombinant OP-metabolizing enzyme, OPAA, resulting in prolongation of enzymatic concentration in the body. These studies suggest that the protection of OP intoxication can be strikingly enhanced by adding OPAA encapsulated within (SL)* to pralidoxime and atropine.     

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.