高效液相色谱法测定卡马西平片的含量

建立卡马西平片含量测定的HPLC方法。色谱柱为LichrosorbDiol (4 0× 2 5 0mm ,5 μm ) ;流动相 :乙腈 -甲醇 - 0 0 5 %冰醋酸溶液 (5∶5∶90 ) ;流速 :1 0ml·min-1;检测波长 :2 30nm ;柱温 :2 5℃ ;峰面积外标法。卡马西平在 10～ 10 0 μg·ml-1范围内具有良好的线性关系 ,回归方程为A =1 6 95 3× 10 4C - 2 5 5 5 5× 10 3 ,r=0 99997;平均回收率为 99 6 9% ,RSD =0 75 % (n =6 )。本法准确可靠 ,专属性强 ,能更好地控制其质量。     

HPLC法测定茵栀黄软胶囊中黄芩苷、栀子苷和绿原酸的含量

目的测定茵栀黄软胶囊中的 3种有效成分 ,黄芩苷、栀子苷、绿原酸的含量。方法HPLC法 ,Irregular HC18(2 5 0 . 0mm× 4 6mm ,10 μm)色谱柱。黄芩苷流动相 :甲醇 水 磷酸 (V∶V∶V =4 7. 0∶5 .3 0∶0. 2 ) ,流速 :1 0mL·min-1,检测波长 :2 80nm ;栀子苷流动相 :乙睛 水 (V∶V =15∶85 ) ,流速 :1 0mL·min-1,检测波长 :2 38nm ;绿原酸流动相 :乙睛 磷酸溶液 (w =0 . 4 % )(V∶V =13∶87) ,流速 :1 0mL·min-1,检测波长 :32 7nm。结果黄芩苷在 2 7 5～ 137 5mg·L-1内质量浓度与峰面积具有良好的线性关系 ,线性回归方程为A =6 4. 83× 10 4ρ - 1 6. 96× 10 .5 ,r =0 . 9998,平均回收率为 99 4 6 % (RSD =1 0 1% ) ;栀子苷在 16 .5～ 82 . 5mg·L-1内质量浓度与峰面积具有良好的线性关系 ,线性回归方程为A =8 794× 10 .5ρ - 4 . 116× 10 2 ,r =0 . 9999,平均回收率为 10 0 . 37% (RSD =1 4 .0 % ) ;绿原酸在 2 4～ 12 0mg·L-1内质量浓度与峰面积具有良好的线性关系 ,线性回归方程为A =2 4 88× 10 4ρ - 9 2 4 4× 10 4,r =0 9999,平均回收率为 99 38%(RSD =1. 89% )。结论测定方法可用于茵栀黄软胶囊的质量控制。     

高效液相色谱法测定结肠安灌肠剂中芍药苷的含量

目的 :应用高效液相色谱法对结肠安灌肠剂中芍药苷进行含量测定。方法 :选用HypersilODS - 2分析柱(2 5 0mm× 4 6mm ,5 μm) ,乙腈 - 0 0 5mol·L-1磷酸二氢钾 (13∶87)为流动相 ,检测波长为 2 30nm ,流速 1 0mL·min-1。结果 :线性范围为 1 12～ 6 72 μg (r =0 99999) ,平均回收率为 97 6 3% ,RSD为 0 85 %。结论 :本法简便、灵敏、准确     

HPLC法测定心痛康胶囊中芍药苷含量

目的　测定心痛康胶囊中芍药苷含量。方法　选用HypersilODS - 2分析柱(2 5 0mm× 4 6mm,5 μm),乙腈 -磷酸盐缓冲液(10∶6 5)为流动相,检测波长为 2 30nm,流速为 1 0ml·min-1,柱温为室温;结果　线性范围为 1 12～ 6 72 μg(r =0 9998),平均回收率为 98 6 5 %,RSD为 0 78%(n =5),结论　该法简便、灵敏、准确。     

HPLC法测定血府逐瘀软胶囊中芍药苷与甘草酸的含量

目的　建立高效液相色谱法测定血府逐瘀软胶囊中芍药苷与甘草酸的含量测定方法。方法　采用 Kro-masil C18(2 0 0 mm× 4 .6 mm ,5μm)色谱柱 ;流动相为甲醇 -水 (30∶ 70 ) ,检测波长 2 30 nm ,用于测定芍药苷 ;流动相为乙腈 - 10 m L· L-1醋酸 (35∶ 6 5 ) ,检测波长 2 5 0 nm,用于测定甘草酸。结果　线性范围分别为 :芍药苷0 .4 8～ 2 .4 μg,r =0 .9999(n =5 ) ;甘草酸 0 .5 15 2～ 2 .5 76 μg,r =0 .9999(n =5 )。平均回收率 ,芍药苷为98.9% ,RSD =1.8% (n =6 ) ;甘草酸 10 0 .3% ,RSD =1.7% (n =6 )。结论　本法分离度好 ,快速 ,简便     

高效液相色谱法测定黄芩颗粒剂中黄芩苷的含量

目的　建立一种黄芩颗粒剂中黄芩苷的含量测定方法。 方法 　黄芩颗粒剂用 70 %乙醇 3 0 min超声提取黄芩苷 ,经稀释后作为供试品溶液。采用 HPL C法测定黄芩苷的含量。YWG-C1 8反相柱 ( ODS) ,4.6mm× 2 5 mm( 5 μm) ,甲醇 -水 -磷酸 ( 4 7∶ 5 3∶ 0 2 )为流动相 ,检测波长 λ=2 80 nm。 结果 　黄芩苷在 0 .14 8～ 2 .96μg范围内 ,线性关系良好 ,回归方程 :Y=2 2 18.47+2 999870 .0 7X,r=0 .9997。加样平均回收率为98.68%,RSD=2 .60 %。 结论 　该方法简单 ,灵敏度高 ,测定结果准确稳定 ,可作为黄芩颗粒剂的质量控制方法     

HPLC法测定银黄含化片中绿原酸和黄芩苷含量

目的　建立HPLC法测定银黄含化片中绿原酸和黄芩苷含量。方法　采用C18柱(2 5 0mm× 4 6mm,5 μm),乙腈 -1%乙酸(30∶70)为流动相,流速为 1ml·min-1,检测波长 0～ 5min,32 7nm,测定绿原酸;5～ 10min,2 80nm,测定黄芩苷。结果　绿原酸在 0 14 4～ 0 72 μg范围内峰面积与进样量呈良好的线性关系,RSD =0 5 5 %(n =6);黄芩苷在 0 2 5～ 1 2 5 μg范围内峰面积与进样量呈良好的线性关系,RSD =0 6 5 %(n =6)。     

高效液相色谱法测定参芍胶囊芍药苷的含量

目的　建立反相高效液相色谱法测定参芍胶囊中芍药苷的含量。方法 　本品以甲醇 -水 (1∶ 1)超声振荡提取 ,提取物滤过、离心后 ,进行高效液相色谱分析。色谱柱 Extend-C1 8(5 μm.4.6× 2 5 0 mm) ;流动相为甲醇 -水 -乙腈 (10∶ 75∶ 15 ) ;流速 :1.0 ml·min- 1 ;柱温 :3 0℃ ;检测波长 :2 3 0 mm。结果 　平均加样回收率为 99.0 3～ 99.5 4% ,RSD为 1.5～ 2 .1% (n=6)。 结论 　实验结果表明 ,该法操作简便、重现性好 ,可作为样品的检测方法     

高效液相色谱法测定排石灵片中芍药苷的含量

目的 :建立一种排石灵片中芍药苷的含量测定方法。方法 :采用高效液相色谱法。色谱柱为HypersilODSC18(4 .6mm× 2 5 0mm ,5 μm) ;流动相 :甲醇 水 (2 8∶72 ) ;流速 :1mL·min-1;柱温 :2 5℃ ;检测波长 :2 30nm。结果 :进样量在 0 .2 5～ 6 .2 5 μg内呈现良好的线性关系 ,回归方程为Y =6 .0 89× 10 -5X +0 .10 87,r =0 .9999,平均回收率为 98.4 % ,RSD为 1.6 %(n =5 )。结论 :测定方法简便 ,准确 ,重现性好 ,适合于排石灵片的含量测定     

高效液相色谱法测定康媛颗粒中阿魏酸的含量

建立高效液相色谱法测定康媛颗粒中阿魏酸的含量。色谱柱LichrospherC18(5 μm ,2 5 0mm×4 6mm) ,流动相 :甲醇 - 0 16 %醋酸溶液 (38∶6 2 ) ;检测波长 :32 3nm ;阿魏酸的线性范围为 7～ 35 μg·ml-1(r=0 9995 ) ,平均回收率为 96 89% ,RSD为 1 34% (n =5 )。本法操作简单 ,快速 ,准确 ,可行。     

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.     

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.