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排序方式: 共有127条查询结果,搜索用时 140 毫秒
41.
Gas chromatographic analysis of norcantharidin and related compounds using derivatization to imides 总被引:1,自引:0,他引:1
Derivatization to imides has been studied for determining ,β-diacids or corresponding anhydrides (e.g. norcantharidin) as well as for analysing primary amines by gas chromatography. 2-Naphthylaniline, n-heptylamine, cyclohexamine, 2,5-dimethoxyaniline, 2,4,5-trichloroaniline, 3,5-dichloroaniline, aniline and benzylaniline were used as derivatization reagents. 1H-nuclear magnetic resonance and mass spectrometry data were obtained for the norcantharidin N-imides synthesized. Factors such as derivatization yields, linearity, reproducibility and sensitivity were evaluated. The influences of reaction temperature and solvent were investigated. 相似文献
42.
目的 建立去甲斑蝥素体外肝细胞代谢产物的HPLC-MS分析方法。方法 去甲斑蝥素进行体外肝细胞代谢,透析得到代谢产物,并用HPLC-MS对产物进行鉴定,再通过半制备HPLC色谱仪分离纯化,最后根据理化性质和波谱数据鉴定代谢物的结构。结果 共分离得到7个化合物,对其中量较高的2个化合物进行结构鉴定,分别为去甲斑蝥素与谷氨酸结合物(1)、去甲斑蝥酸钠(2)。结论 体外细胞代谢法由于反应条件相对单纯,易于控制,适合于制备去甲斑蝥素体外肝细胞代谢产物。 相似文献
43.
目的:制备去甲斑蝥素(NCTD)脂质体并探讨其药剂学性质。方法:采用逆向薄膜蒸发法制备NCTD-脂质体,并采用正交设计优化处方工艺,利用平衡透析法对含NCTD的载药脂质体进行体外释放的评价。结果:影响包封率和粒径的因素,依次为A>C>B,各因素组合以A2C1B2最佳,即磷脂-药物质量比为10∶1,磷脂-胆固醇质量比为5∶1,超声次数为10次;制得的NCTD-脂质体的粒径为(90.50±2.40)nm,包封率为(34.7±1.3)%,实验结果显示缓释效果明显。结论:逆向薄膜蒸发法制备的NCTD-脂质体,其性质稳定,具有显著的体外缓释特性。 相似文献
44.
去甲斑蝥素复方注射液联合CTOP方案治疗淋巴瘤疗效观察 总被引:1,自引:0,他引:1
目的观察比较去甲斑蝥素复方注射液联合CTOP(环磷酰胺+吡喃阿霉素+长春新碱+强的松)方案化疗与单用CTOP方案化疗对非霍奇金淋巴瘤的疗效及不良反应。方法 57例非霍奇金淋巴瘤患者分为两组,观察组以去甲斑蝥素复方注射液60~80mL+5%葡萄糖500mL静脉滴注,1次/d,疗程为14d,联合标准CTOP方案化疗。对照组单用标准CTOP方案化疗。治疗2个疗程后,两组进行疗效、生活质量及不良反应评定。结果两组的治疗有效率分别为,观察组70.83%,对照组63.63%,疗效差异无统计学意义;但比起对照组,观察组患者生活质量提高、化疗不良反应减轻情况差异有统计学意义(P<0.05)。结论去甲斑蝥素复方注射液联合化疗较单用化疗疗效无明显差异;但更有利于提高患者生活质量,减轻化疗不良反应。 相似文献
45.
目的探讨去甲斑蝥素(NCTD)对微管蛋白聚合-解聚过程的影响。方法采用蛋白凝胶电泳鉴定从猪脑中提取的微管蛋白,并用Bradford法测定微管蛋白含量。在经过秋水仙碱和紫杉醇验证稳定的37℃和4℃平衡体系内加入NCTD 10,20和30μmol.L-1观察微管蛋白聚合-解聚活性。人卵巢癌SK-OV-3细胞加入NCTD 60μmol.L-1作用8 h,取上清和沉淀,Western印迹法检测微管蛋白含量。结果与空白对照组相比,在37℃聚合反应中,NCTD 10,20和30μmol.L-1组对微管蛋白聚合的抑制率分别为(5.5±2.7)%,(7.1±1.2)%和(27.5±0.4)%,在此浓度范围内NCTD随浓度的升高抑制作用增强(P<0.05),但对微管蛋白在4℃的解聚影响不显著。NCTD 60μmol.L-1作用人卵巢癌细胞后,细胞中游离微管蛋白增加了(91.5±8.5)%,聚合微管蛋白量减少了(51.8±3.8)%,说明NCTD抑制了人卵巢癌细胞SK-OV-3中微管蛋白的聚合。结论 NCTD对体外微管蛋白的聚合具有一定的抑制作用。 相似文献
46.
《Expert opinion on therapeutic patents》2013,23(11):1743-1753
Introduction: Norcantharidin (7-oxabicyclo [2.2.1] heptane-2,3-dicarboxylic anhydride) is the demethylated form of cantharidin. Norcantharidin not only has strong anticancer activity, but also eliminates most side-effects in the urinary system, does not cause myelosuppression and increases the number of white blood cells. With structural modification, norcantharidin analogues show potential anticancer activities. Areas covered: A comprehensive patent review of norcantharidin analogues from 2006 to 2010 is presented. Protein phosphatase 1, 2A, 2B and 5 inhibitors are described. The review summarizes the new compounds and lays the foundation for seeking more effective anticancer compounds. Expert opinion: Although norcantharidin has improved activity and toxicity, the effects routinely do not satisfy the current clinical need. Exploring better analogues is vital for changing the current situation, but norcantharidin is a good lead compound. 相似文献
47.
目的:制备去甲斑蝥素壳聚糖-丝素蛋白栓塞微球(Norcantharidin-loaded chitosan-fibroin micro-spheres for embolization,NCTD-CS-SF-MS),考察其包封率,载药量及外观形态,并对其体外释放特性进行考察。方法:采用乳化-交联固化法制备NCTD-CS-SF-MS,其中以液体石蜡为油相,壳聚糖(chitosan CS)与丝素蛋白(silk fibroin SF)的物理混合溶液为水相,Span-80为乳化剂,戊二醛为交联剂。星点设计-效应面法优化制备工艺,扫描电镜观察微球表面形态及X-射线衍射(XRD)、差示量热扫描(DSC)表征微球特性。采用体外动态透析法测定微球在不同介质条件下的释药性能。结果:制备的微球形态圆整,大小均匀,平均粒径约(184±5)μm,载药量(15.08±2.85)%,包封率(27.46±1.25)%。微球在0.1 mol.L-1 HCl、PBS(pH=7.4)和生理盐水中的释放均遵循Weibull方程。结论:所优化的制备工艺简单易行,缓释作用显著。 相似文献
48.
目的 明确去甲斑蝥素 (norcantharidin, NCTD) 对肿瘤细胞周期的影响,进一步阐明 NCTD 的抗肿瘤作用机制。方法 体外培养 HL-60 细胞,NCTD 作用后采用3H-TdR 掺入实验检测 DNA 复制;流式细胞术检测细胞周期进程;Western blotting 检测细胞周期调控蛋白 Cdk1、Cyclin B1、Cdc 25c 表达变化。结果 不同浓度 (16~128 μmol/L) NCTD 作用于 HL-60 细胞 12 h 后,DNA 复制受到抑制,细胞周期出现明显的 S 期累积,并呈剂量依赖性趋势;同时观察到 G2/M 的阻滞,且调控 G2/M 周期进程的调节蛋白 Cdk1、Cyclin B1 及 Cdc 25C 蛋白表达下调。结论 NCTD 可抑制 HL-60 细胞 DNA 复制、下调周期调控蛋白从而干扰肿瘤细胞的周期进程。 相似文献
49.
Objective: To investigate the mechanism of norcantharidin (NCTD)-induced SMMC-7721 hepatoma cell apoptosis. Methods: SMMC-7721 cell growth inhibition was measured by the MTT method. Apoptosis was detected by Annexin Ⅴ/propidium iodide staining. The mitochondrial membrane potential was measured by flow cytometry. Western blot analysis was used to evaluate the level of cytochrome c, caspase-3, AIF, Bcl-2 and Bax expression. Results: NCTD inhibited SMMC-7721 cell growth in a time-and dose-dependent manner. The cells treated with NCTD showed the loss of mitochondrial membrane potential. The activities of caspase-3, cytochrome c, AIF, and Bax were up-regulated after NCTD treatment at different doses. The expression of Bcl-2 was decreased after treatment with NCTD. Conclusions: NCTD could induce SMMC-7721 cell apoptosis. The activation of the mitochondrial pathway was involved in the process of NCTD-induced SMMC-7721 cell apoptosis. 相似文献
50.
Hui-Fen Liao Yu-Jen ChenChin-Hung Chou Fang-Wei WangCheng-Deng Kuo 《Toxicology in vitro》2011,25(1):206-212
Norcantharidin (NCTD) is a potential anti-cancer agent that inhibits proliferation and induces cell death through regulation of mitogen-activated protein kinases (MAPK). This study examined the effect of NCTD on tumor cells by using a model of phorbol 12-myristate 13-acetate plus ionomycin (PMAI)-activated leukemia Jurkat T cells. The results showed that NCTD significantly inhibited the viability of cells with and without PMAI treatment. NCTD induced cell cycle arrest at G2/M phase, down-regulated the expression of calcineurin and, by itself or in combination with Cyclosporine A, reduced calcineurin phosphatase activity. Furthermore, NCTD up-regulates the expression of phosphorylated (p)-P38 and p-ERK1/2, but not JNK in PMAI-activated Jurkat T cells, in accordance with the alteration in viability. Regarding major cytokine and chemokine secretion profile, NCTD attenuates PMAI-augmented production of IL-2, but slightly increases or has no effect on TNF-α and IL-8. By blockade of various MAPK, NCTD regulates PMAI-augmented IL-2 production through activation of P38 and ERK1/2, in accordance with the aforementioned MAPK expression. In conclusion, NCTD inhibited IL-2 production in PMAI-activated human leukemia Jurkat T cells through activation of P38 and ERK1/2, suggesting that NCTD might have the potential of being used as a chemopreventive agent to inhibit tumor progression in the future. 相似文献