细叶桉叶超临界CO_2萃取挥发油的GC-MS分析

目的:分析经超临界CO(2SFE-CO2)萃取的细叶桉叶挥发油的化学成分。方法:采用SFE-CO2法从细叶桉叶中提取挥发油,用气相色谱-质谱联用技术对其化学成分进行分析,并用归一化法确定各化学成分的相对百分含量。结果:细叶桉叶挥发油中共提取、鉴定出28种化合物,占色谱峰总面积的88.13%。其挥发性组分主要是桉油精(33.99%)、冰片(8.88%)、α-蒎烯(5.39%)、石竹烯(4.51%)、(+)-4-蒈烯(4.19%)等。结论:本研究可为细叶桉叶的进一步开发利用提供科学依据。     

广西黄皮叶挥发油化学成分GC-MS分析研究

目的:对广西黄皮叶挥发油进行气相-质谱研究.方法:利用水蒸气蒸馏法提取广西黄皮叶挥发油,采用气相色谱-质谱联用法鉴定化学成分,归一化法测定各成分相对含量.结果:从广西黄皮叶挥发油中共分离出40多个组分,鉴定了其中32个化合物,占总量的90%以上,主要成分为石竹烯(25.31%)、石竹烯氧化物(14.86%)、β-红没药烯(8.95%)、斯巴醇(8.88%)、柏木-8(15)-烯-9-醇(7.54%)、α-法呢烯(6.51%)等,并鉴定出12种文献未见报道的组分.结论:广西黄皮叶挥发油中含倍半萜醇类、倍半萜烯类及其含氧衍生物等多种化学成分,本试验为广西黄皮叶的进一步开发利用提供了科学依据.     

固相微萃取GC-MS法分析大唇香科科、二齿香科科、长毛香科科的挥发油成分

目的:对大唇香科科、二齿香科科、长毛香科科的挥发油成分进行分析。方法:采用固相微萃取技术提取挥发油成分,用气相色谱-质谱联用技术对挥发油进行分析测定。结果:从大唇香科科、二齿香科科挥发油中共鉴定出33个化学成分,其中含量较高的组分为大栊牛儿烯-D(26.66%、27.88%)、1-辛烯-3-醇(13.19%、13.79%)、α-蒎烯(12.53%、13.07%)、β-芹子烯(5.93%、6.08%)、大栊牛儿烯-B(5.89%、6.20%)等。从长毛香科科挥发油中共鉴定出29个化学成分,其中含量较高的组分为石竹烯氧化物(21.52%)、α-甜没药萜醇(20.35%)、α-蒎烯氧化物(18.25%)、1-辛烯-3-醇(7.26%)、α-甜没药萜醇氧化物B(5.92%)等。结论:本试验可为香科科属植物资源的开发利用提供理论依据。     

兴安杜鹃中挥发油的气质联用分析

目的:用气相色谱-质谱法对兴安杜鹃挥发油进行成分分析。方法:采用水蒸气蒸馏法从兴安杜鹃中提取挥发油,然后经毛细管色谱柱进行分离,用归一化法计算含量。色谱条件:HP-1石英毛细管柱(30 m×0.32 mm,0.25μm),柱温条件:起始温度110℃(20 min)、4℃·min~(-1)140℃(7min)7℃·min~(-1)220℃(10 min):分流进样.分流比1:60:进样口温度280℃;MS检测器。结果:挥发油中共鉴定出29个化合物,占挥发油总量的93.01％。主要成分是:α-石竹烯(26.07％),α-律草烯(17.36％),α-芹子烯(8.06％)β-芹子烯(7.05％),γ-杜松烯(4.82％),δ-杜松烯(3.90％),杜松烯(2.28％),α-松油醇(1.51％),檀香醇(1.12％)。结论:本法可靠,可用于测定从兴安杜鹃中提取的挥发油。     

狭叶羌活根茎和根的挥发油成分的GC-MS分析

目的分析狭叶羌活(Notopterygium incisumTing ex H. T. Chang)根茎和根的挥发油的化学成分,为其质量评价提供科学依据。方法采用水蒸气蒸馏法提取狭叶羌活根茎和根的挥发油,用GC毛细管柱进行分析,归一化法测定其相对含量,并用GC-MS法鉴定化学成分。结果检出242个色谱峰,初步鉴定出83个化合物,占挥发油总量的75·77%。结论狭叶羌活根茎和根的挥发油中的化学成分主要为单萜和倍半萜类化合物,两者分别占总油中化学成分的13·63 %和67.93 %。(1S)-β-蒎烯(1·67%)、3-蒈烯(1·05%)、柠檬烯(1·22%)和1S-endo-醋酸冰片酯(1·68%)为单萜类化合物中的主要成分;( )-β-榄香烯(6·78%)、苜蓿烯(1·54%)、α-石竹烯(2·64%)、异大香叶烯D (1·67%)、桉烷-4 (14),11-二烯(2·36%)、α-芹子烯(2·42%)、δ-杜松烯(1·55%)、3,7,11-三甲基-2,6,10-十二烷三烯-1-醇(1·03%)、(±)-榄香烯(5·18)、(-)-匙叶桉油烯醇(1·40%)、愈创醇(3·81%)、去羟基异菖蒲烯二醇(1·06%)、γ-桉醇(1·05%)、α-桉醇(7·97%)、异愈创木醇(3·09%)和胡萝卜醇(2·30%)为倍半萜类化合物中的主要成分。总挥发油中,反式肉桂酸异丙酯占11·3%,为所有化合物中含量最高者。     

GC-MS分析壮药大头陈中的挥发油成分

目的:研究大头陈挥发油的成分。方法:应用GC-MS法分析大头陈中的香挥发油成分。结果:从大头陈挥发油中分离出57个组分,确认了其中的50种成分,主要成分为异松油烯(27.84%)、柠檬烯(24.72%)、1,8-桉叶素(8.22%)、α-蒎烯(6.04%)、α-石竹烯(6.23%)和β-石竹烯(5.93%)等。结论:所有化合物均为从该植物中首次鉴定出,其中37个成分系从该属植物中首次鉴定出。     

朝鲜苍术挥发油成分GC—MS分析

目的研究朝鲜苍术挥发油成分,为朝鲜苍术的药用价值及合理开发利用提供参考。方法采用水蒸气蒸馏法提取挥发油,GC毛细管柱色谱法进行分析,峰面积归-化法确定其相对含量,气相色谱-质谱联用技术辅助人工检索鉴定其化学成分。结果从朝鲜苍术的挥发油中分离出58种,鉴定出55种化学成分,鉴定出的挥发性化学成分占挥发油总量的79．94％,主要成分有苍术酮（31．1831％）、3-羟基-6β-环丙烷-5β-胆甾烷（12．3086％）、5α-螺甾烷（11．2161％）、巴伦西亚橘烯（7．05606％）、γ-榄香烯（4．24732％）、菜油甾醇（2．11089％）、石竹烯（1．44473％）、β-桉叶烯（1．43541％）、9,10-脱水-异长叶烯（1．21445％）、α-石竹烯（0．72132％）。结论朝鲜苍术挥发油的主要化学成分为倍半萜类化合物。     

藏药木橘挥发油化学成分气相色谱-质谱联用分析

目的 促进藏药木橘的开发利用.方法 采用水蒸气蒸馏法提取挥发油,峰面积归一化法测定相对含量,气相色谱-质谱联用技术(GC-MS)辅助人工检索鉴定其化学成分.结果 共分离和鉴定了33个化合物,占挥发油总量的91.82％,其中脂肪酸类相对百分含量为51.97％.藏药木橘挥发油的主要成分为棕榈酸(40.04％),β-石竹烯(10.04％),油酸(7.83％),香叶烯B(5.33％),α-葎草烯(3.53％),γ-姜黄烯(2.61％)和α-桉叶烯(2.30％)等.结论 藏药木橘具有较好的药物开发潜质,值得深入研究.     

伸筋草挥发油成分的固相微萃取分析

目的：分析伸筋草中挥发油化学成分。方法：采用固相微萃取气相色谱-质谱联用法分析挥发油化学成分。结果：共分离出98个组分，鉴定了81个组分，用归一化法测定其百分含量，占总挥发油组分峰面积的97．80％。结论：主要成分是癸酸（10．63％）、β-马榄烯（6．60G）、反-石竹烯（7．29％）、白菖蒲油烯（23．77％）、旷古芸烯（3．38％）、α-姜黄烯（1．38％）、α-蛇床烯（1．67％）、δ-杜松烯（2．16％）、α-雪松醇（15．50％）等组分。     

沙田柚幼果挥发油成分的气相-质谱联用分析

目的:分析沙田柚幼果挥发油成分.方法:用水蒸气蒸馏法提取沙田柚幼果挥发油,用气相-质谱联用(CC-MS)法对挥发油成分进行分析.结果:共分离出33个组分,经NIST谱库检索,鉴定了其中24个化合物,并用峰面积归一化法确定了其相对含量.结论:沙田柚幼果挥发油主要成分有:香芹酚(29.79%)、D-柠檬烯(29.02%)、β-石竹烯(19.27%)、α-佛手柑烯(7.69%)、β-月桂烯(4.61%)、α-石竹烯(2.31%)、奴卡酮(1.91%)等.     

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.