HPLC法测定止咳枇杷糖浆中苦杏仁苷的含量

目的:建立止咳枇杷糖浆中苦杏仁苷的HPLC测定方法。方法:采用Welch(月旭)Ultimate XB-C18(4.6x250mm,5μm),以甲醇-水(20∶80)为流动相,流速1mL/min,检测波长210nm。结果:苦杏仁苷在9.61~153.8μg/mL线性关系良好,线性回归方程Y=0.2716x-1.36466,r=0.9962,平均回收率95.18%。结论:该方法分离度、线性关系、重现性、稳定性、回收率均符合含量分析要求,适合于止咳枇杷糖浆中苦杏仁苷的含量测定。     

风热感冒颗粒中苦杏仁苷和绿原酸及连翘苷的多波长HPLC法含量测定

目的:建立风热感冒颗粒中苦杏仁苷、绿原酸以及连翘苷多波长HPLC的含量测定方法。方法:采用SHISEIDO capcell pak-C_(18)(4.6 mm×250 mm,5μm)色谱柱,以甲醇-0.1%磷酸溶液为流动相,梯度洗脱,流速为1 mL/min,柱温为35℃,进样量为10μL;采用多波长HPLC法分别测定风热感冒颗粒中苦杏仁苷、绿原酸以及连翘苷的含量,检测波长为207 nm(苦杏仁苷)、327 nm(绿原酸)、279 nm(连翘苷)。结果:苦杏仁苷、绿原酸和连翘苷浓度分别在0.171 4~2.571 0μg/mL、0.020 0~0.300 8μg/mL和0.189 1~2.83 7μg/mL范围内呈良好的线性关系(r=0.999 9,0.999 7,0.9998);平均加样回收率分别为98.36%、98.88%和97.21%(n=6);样品中平均含量分别为2.099 mg/g、0.201 mg/g和1.558 mg/g。结论:所建立的多波长HPLC测定法简便、准确,重复性好,专属性强,可有效地用于风热感冒颗粒的质量控制。     

RP-HPLC法同时测定加味补阳还五汤剂中4种成分的含量

目的:建立同时测定加味补阳还五汤剂中芍药苷、苦杏仁苷、阿魏酸、川芎嗪含量的方法。方法:采用反相高效液相色谱法。色谱柱为YMC C18,流动相为乙腈-0.1%磷酸溶液(梯度洗脱),流速为1.0 m L/min,检测波长为320 nm(阿魏酸)、230 nm(芍药苷)、207 nm(苦杏仁苷)、280 nm(川芎嗪),柱温为30℃,进样量为10μL。结果:芍药苷、苦杏仁苷、阿魏酸和川芎嗪检测质量浓度线性范围分别为0.191 2~1.912μg/m L(r=0.999 6)、0.117 4~1.174μg/m L(r=0.999 6)、0.011 5~0.115μg/m L(r=0.999 8)和0.001 66~0.016 6μg/m L(r=0.999 7);定量限分别为1.912、1.174、0.115、0.016 6μg/m L,检测限分别为0.25、0.40、0.05、0.008 5μg/m L;精密度、稳定性、重复性试验的RSD<2.0%;加样回收率分别为96.9%~100.3%(RSD=1.3%,n=6)、95.1%~100.3%(RSD=2.2%,n=6)、95.3%~100.2%(RSD=2.0%,n=6)、97.0%~100.0%(RSD=1.3%,n=6)。结论:该方法可靠、简便、准确,适用于同时测定加味补阳还五汤剂中芍药苷、苦杏仁苷、阿魏酸、川芎嗪的含量。     

高效液相色谱法测定止咳宁嗽胶囊中苦杏仁苷含量

目的建立测定止咳宁嗽胶囊中苦杏仁苷含量的高效液相色谱法。方法用Zorbax Eclipse XDB-C18色谱柱(150 mm×4.6 mm,5μm),流动相为甲醇-水(20∶80),检测波长为218 nm,流速为1.0 mL/min。结果苦杏仁苷的质量浓度线性范围为7.16～71.6μg/mL(r=0.999 5),平均回收率为99.21%,RSD为0.48%(n=6)。结论该方法专属性强、操作简便,可用于产品的质量控制。     

高效液相色谱法测定小儿麻甘颗粒中苦杏仁苷的含量

目的建立测定小儿麻甘颗粒中苦杏仁苷含量的高效液相色谱法。方法采用Kromasil C18(250mm×4.6mm,5μm)色谱柱,流动相:甲醇-水-磷酸(17∶83∶0.1,v/v/v),流速:1.0mL/min,检测波长:210nm,柱温:35C。结果苦杏仁苷在0.3602～5.406μg(r=0.9999,n=8)浓度范围内与峰面积呈良好线性关系;精密度试验RSD为1.4%;重复性试验RSD为0.89%;稳定性试验RSD为1.5%;平均加样回收率(n=9)为99.3%(RSD=0.95%)。结论本测定方法简便、快捷、准确,为小儿麻甘颗粒质量评价提供依据。     

郁李仁配方颗粒的质量标准研究

目的:建立郁李仁配方颗粒的质量标准。方法:采用薄层色谱(TLC)法对郁李仁配方颗粒中的苦杏仁苷进行定性分析,采用高效液相色谱(HPLC)法测定制剂中苦杏仁苷的含量。色谱柱为GP-Phenyl,流动相为乙腈-水(10∶90,V/V),流速为0.8 ml/min,检测波长为210 nm,柱温为30℃,进样量为5μl。结果:苦杏仁苷的TLC图斑点清晰、分离较好,阴性对照无干扰。苦杏仁苷质量浓度在50.92~611.04μg/ml范围内与其峰面积积分值呈良好线性关系(r=0.999 8);精密度试验的RSD<2%,稳定性、重复性试验的RSD<3%;平均加样回收率为101.07%,RSD为0.64%(n=6)。结论:该方法操作简单、灵敏、专属性强、重复性好,可作为郁李仁配方颗粒的质量控制方法。     

RP-HPLC法测定小儿清肺化痰口服液中苦杏仁苷的含量

目的 建立RP-HPLC法测定小儿清肺化痰口服液中苦杏仁苷含量的方法 .方法采用反相高效液相色谱法,Diamonsil-C18柱,以甲醇-0.1%磷酸水溶液(10:90,v/v)为流动相,流速为1.0mL·min-1,检测波长为215nm,柱温为室温.结果 苦杏仁苷浓度在4~48μg·mL-1间具有良好的线性关系(r=0.9995),平均回收率为103.4%,方法精密度(RSD)为0.90%(n=6).结论 该法可用于小儿清肺化痰口服液中苦杏仁苷的含量测定.     

高效液相色谱法测定橘红丸中苦杏仁苷的含量

目的建立HPLC法测定橘红丸中苦杏仁苷的含量。方法以甲醇-水（15：85,v/v）为流动相;在phenomenex Luna C18（2）（200 mm×4.6 mm,5μm）色谱柱上测定苦杏仁苷的含量,流速为1.0 mL min-1,检测波长为210 nm。结果苦杏仁苷在0.53～5.3μg与峰面积线性关系良好（r=0.999 9）,平均回收率为96.8%,RSD=1.2%。结论本法简便、可靠、准确,结果满意。     

HPLC法测定小儿清热止咳口服液中苦杏仁苷的含量

目的建立小儿清热止咳口服液中苦杏仁苷含量的测定方法.方法采用高效液相色谱法,Diamonsil-C18柱(250mm×4.6mm,5μm),甲醇-0.1%磷酸溶液(10∶90)为流动相,流速为1.0mL·min-1,检测波长为210 nm.结果苦杏仁苷浓度在4～48μg·mL-1间具有良好的线性关系(r=0.999 5),苦杏仁苷平均回收率为98.6%,RSD为1.86%(n=6).结论本法简便、准确、重现性好,可以用于小儿清热止咳口服液中苦杏仁苷的质量控制.     

高效液相色谱法同时测定三拗片中盐酸麻黄碱和苦杏仁苷的含量

目的建立高效液相色谱同时测定三拗片中盐酸麻黄碱和苦杏仁苷含量的方法。方法采用Hypersil BDSC18柱(250 mm×4.6 mm,5μm),流动相为甲醇-0.3%磷酸溶液(20∶80),检测波长为217 nm,流速为1.0 mL.min-1,柱温为30℃,外标法计算含量。结果盐酸麻黄碱在0.019 9~0.398μg与峰面积有良好的线性关系,r=0.999 8,平均回收率为97.6%,RSD为1.2%(n=9);苦杏仁苷在0.104 2~2.084μg与峰面积有良好线性关系,r=0.999 9,平均回收率为98.2%,RSD为1.0%(n=9)。结论该方法简便、准确、重复性好,可同时测定三拗片中盐酸麻黄碱和苦杏仁苷的含量。     

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.