微波法制备甘露糖醛酸寡糖及其抗氧化活性研究Δ

目的 制备分离不同聚合度的甘露糖醛酸寡糖单体,测定其体外抗氧化活性。方法 采用微波辅助降解法,制备甘露糖醛酸寡糖混合物,采用Bio Gel P-6凝胶渗透色谱法对寡糖混合物进行分离纯化,得到7个寡糖组分;运用薄层色谱法(HPTLC)、荧光辅助糖电泳法(FACE)、红外光谱法(IR)、质谱法(MS)对不同组分进行分析;比较不同寡糖组分对羟基自由基、超氧自由基、DPPH自由基的清除作用及对亚铁离子络合作用的差异。结果和结论 采用微波辅助法能够实现对聚甘露糖醛酸的可控降解,通过对寡糖混合物进行分离纯化获得7个组分,分别为聚合度为1~7的饱和甘露糖醛酸寡糖。体外抗氧化研究表明,甘露糖醛酸寡糖具有清除DPPH、羟基自由基、超氧自由基及络合亚铁离子的能力,其活性与寡糖聚合度有关。清除DPPH、超氧自由基及络合亚铁离子的能力随着寡糖单体聚合度增大而降低;清除羟基自由基的能力随着聚合度增加而升高。     

半枝莲多糖的提取纯化及抗氧化活性研究

目的研究半枝莲多糖的分离纯化及抗氧化作用。方法采用正交试验L9(34)对半枝莲多糖提取工艺进行优化,并利用DEAE-Cellulose-52和Sepharose 4B柱色谱进一步纯化多糖组分;分光光度法测定半枝莲多糖对小鼠红细胞溶血、小鼠血清、肝组织中的超氧化物岐化酶(SOD)活力以及过氧化产物丙二醛(MDA)生成的影响。结果半枝莲多糖提取工艺的最佳条件为温度70℃,提取6 h,料水比1∶30,温度是提取多糖的关键影响因素。抗氧化活性实验表明半枝莲多糖的两个组分SBPW、SBPS在一定浓度范围内均能降低化学法诱导的红细胞溶血和肝组织过氧化物损伤;能剂量依赖性提高小鼠血清、肝组织中的SOD活力,降低小鼠血清、肝组织中MDA的水平。结论SBPW和SBPS具有较好的抗氧化作用。     

维吾尔药牛舌草提取物抗氧化活性研究

目的研究维吾尔药牛舌草提取物的抗自由基作用及体内抗氧化功能。方法采用体外分析法观察牛舌草提取物对DPPH·及超氧自由基的清除作用,并进一步针对牛舌草大孔树脂洗脱部位GZB-3及GZB-AB80的提取物,以小鼠血清SOD、GSH-Px的活性和MDA的含量变化,探讨牛舌草提取物在小鼠体内的抗氧化能力。结果牛舌草各提取物具有体外抗自由基功能,其中牛舌草GZB-3及GZB-AB80提取物有较好的清除DPPH·及超氧自由基的作用;牛舌草提取物可显著增强小鼠血清SOD、GSH-Px活性,降低MDA含量,其中GZB-AB80提取物有较好的体内抗氧化能力。结论体内外抗氧化实验表明,牛舌草提取物具有明显的抗自由基作用及抗氧化功能。     

白藜芦醇抑制肺癌Lewis荷瘤小鼠肿瘤生长及其体内外抗氧化活性

目的:研究白藜芦醇体内抑制肺癌瘤块生长活性以及其体内外抗氧化活性。方法:采用肺癌Lewis C57BL/6J小鼠模型评价白藜芦醇的抗肿瘤活性,并测定荷瘤小鼠血清中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量;采用活性氧(ROS)荧光探针测定白藜芦醇对人非小细胞肺癌SPC-A-1细胞内的ROS含量,并测定培养液中的SOD活性和MDA含量。结果:白藜芦醇能显著抑制体内肺癌瘤块的生长,高、中、低剂量组的抑制率分别为(58.4±5.5)%、(46.9±17.4)%和(31.9±8.1)%。白藜芦醇能上调荷瘤小鼠和SPC-A-1细胞的SOD活性,并降低MDA含量,还降低肿瘤细胞内的ROS含量。结论:结果表明白藜芦醇能抑制体内肺癌瘤块的生长;其抗氧化作用是其抗肺癌的主要机制之一。     

石斛多糖抗氧化活性研究

目的研究石斛多糖的体内、体外抗氧化活性。方法①体外抗氧化实验：用化学反应法检测石斛多糖对邻苯三酚自氧化反应产生的超氧阴离子和Fenton反应产生的羟自由基的清除作用;②体内抗氧化实验：昆明种小鼠随机分为空白对照组、小剂量组、中剂量组和大剂量组,每组10只。研究石斛多糖对小鼠血清及肝组织中SOD、GSH-Px、MDA的影响。结果石斛多糖具有清除羟基自由基和超氧阴离子自由基的作用,可显著提高小鼠血清和肝组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活力,降低丙二醛（MDA）含量。结论石斛多糖具有明显的抗氧化活性,为进一步开发石斛药材提供依据。     

硒化桑葚多糖及其抗氧化活性研究

目的:通过硒化修饰改变桑葚多糖分子结构,并对比研究其体内抗氧化活性.方法:采用水提醇沉法提取桑葚多糖(FMP),硒化修饰FMP,得到桑葚多糖硒化衍生物(FMPs);考察桑葚多糖的体内抗氧化能力,测定小鼠血清和肝脏中MDA、肝脏T-AOC和CAT;建立高脂血症大鼠抗氧化损伤模型,考察FMP及FMPs的抗氧化能力.结果:FMPs及FMP均可以显著提高正常小鼠肝组织CAT活力及T-AOC,降低小鼠血清及肝脏MDA含量,FMPs抗氧化活性明显优于FMP.此外,FMPs及FMP还可以显著降低四氧嘧啶致高脂大鼠的氧化损伤程度,提高其血清SOD活力及肝脏T-AOC,并降低其血清MDA含量.结论:硒化修饰可显著提高桑葚多糖的抗氧化活性.     

玉竹总黄酮体内外抗氧化作用的实验研究

目的研究玉竹总黄酮的体外及其对衰老模型鼠的抗氧化作用。方法用DPPH(对1,1-二苯基苦基苯肼)法测定其体外氧化能力;通过衰老模型小鼠实验来评价其体内抗氧化作用。结果玉竹总黄酮具有较强的抗氧化能力,体外明显抑制DPPH自由基活性,体内明显增强衰老模型小鼠血液中SOD活性,降低肝组织中MDA含量。结论玉竹总黄酮具有明显体内外的抗氧化作用。     

玉竹总黄酮体内外抗氧化作用的实验研究

目的研究玉竹总黄酮的体外及其对衰老模型鼠的抗氧化作用。方法用DPPH（对1，1-二苯基苦基苯肼）法测定其体：氧化能力；通过衰老模型小鼠实验来评价其体内抗氧化作用。结果玉竹总黄酮具有较强的抗氧化能力，体外明显抑制DPF自由基活性，体内明显增强衰老模型小鼠血液中SOD活性，降低肝组织中MDA含量。结论玉竹总黄酮具有明显体内外的抗氧化作用。     

红腺忍冬叶水提物抗氧化作用研究

摘要：目的 研究红腺忍冬叶水提物的抗氧化作用,为红腺忍冬叶的开发利用奠定科学依据。方法 通过对红腺忍冬叶水提醇沉法分离所得各部分的样品进行体内、体外抗氧化的实验研究,从而考察红腺忍冬叶水提物的抗氧化活性。以Vc、二丁基羟基甲苯（BHT）为对照品,通过DPPH法和铁离子还原法考察红腺忍冬叶不同样品的体外抗氧化活性。以Vc为阳性对照,由D-半乳糖（1g/kg）致衰的小鼠为动物模型,通过测定血清、肝脏组织中SOD、GSH-PX活性和MDA含量,考察样品的体内抗氧化活性。结果 红腺忍冬叶水提醇沉分离所得各部分体外抗氧化活性：在 0.1～5mg?mL-1范围内,90%乙醇直接沉淀物,30%乙醇沉淀物以及滤液部分具有较好的抑制DPPH自由基的活性和铁离子还原能力。体内SOD活性影响实验表明：30%乙醇沉淀物高剂量组、90%乙醇直接沉淀物低剂量组对提高小鼠体内SOD活性均有良好的效果,且都略优于Vc,但无显著性差异。体内GSH-PX活性影响实验表明：30%乙醇沉淀物高剂量组、90%乙醇直接沉淀物高剂量组和90%乙醇直接滤液低剂量组为佳。⑤体内MDA含量影响实验表明：30%乙醇沉淀物高、低剂量组和30%乙醇滤液高剂量组以及90%乙醇直接沉淀物低剂量组降低MDA含量的作用最为显著。结论 红腺忍冬叶水提液进一步醇沉分离所得各部分都具有不同程度的抗氧化效果,综合考虑以30%乙醇沉淀物活性最佳,值得进一步研究。     

盐藻β-胡萝卜素抗衰老作用研究

目的观察盐藻β-胡萝卜素(β-C)对果蝇和大鼠的抗衰老作用,并探讨其可能机制。方法①果蝇实验:将果蝇按照不同培养基分组后进行生存实验、性活力实验和飞翔能力实验并测定头部MDA含量。②大鼠实验:老年SD♂大鼠随机分组,灌胃法给药45 d后,测定血浆MDA含量和GSH-Px、CAT活性,以及心、肝、肺、脾、脑MDA含量和SOD、GSH-Px活性。结果①果蝇实验:与对照组相比,各实验组果蝇的平均寿命、最高寿命、最短寿命、延寿率和性活力皆提高,果蝇头部MDA含量减少;②大鼠实验:与对照组相比,各实验组血浆MDA含量明显下降,GSH-Px活性明显增加,心、肝、肺、脾、脑各组织MDA含量皆降低,SOD、GSH-Px活性则皆增加。结论盐藻β-C对果蝇和老年大鼠有抗衰老作用,其可能通过增加体内抗氧化酶的活性,提高机体抗氧化能力而发挥抗衰老作用。     

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.