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中国医师杂志 2010年第10期12卷 1309-1312页

作者：宋淑芳宋静慧张林燕内蒙古医学院第一附属医院妇产科呼和浩特010059

目的探讨第三代芳香化酶抑制剂（aromatase inhibitors,AIs）来曲唑对子宫内膜异位症模型大鼠的作用及对生殖系统的影响.方法应用自体子宫内膜移植方法建立大鼠内异症模型,将20只建模成功大鼠随机分为来曲唑组和盐水对照组,比较治疗... 详细信息

目的探讨第三代芳香化酶抑制剂（aromatase inhibitors,AIs）来曲唑对子宫内膜异位症模型大鼠的作用及对生殖系统的影响.方法应用自体子宫内膜移植方法建立大鼠内异症模型,将20只建模成功大鼠随机分为来曲唑组和盐水对照组,比较治疗前后大鼠子宫内膜异位症（EM）病灶体积的变化;末端转移酶介导的缺口末端标记法（TUNEL）检测细胞凋亡情况;取对侧子宫角及卵巢,称重后行HE染色观察形态学变化.结果来曲唑组异位病灶体积缩小[（28.75±2.28）mm3 vs（108.39±9.98）mm3,P〈0.01];来曲唑组异位内膜细胞凋亡率[（5.52±2.81）%]明显高于对照组[（2.11±1.70）%,P〈0.01];来曲唑组大鼠卵巢重量明显增加[（25.25±9.89）mg/100g vs（13.10±2.70）mg/100g,P〈0.01],卵巢呈多囊样改变;来曲唑组子宫重量减轻[（41.46±15.81）mg/100gvs（94.81±18.00）mg/100g,P〈0.05],内膜呈增生抑制改变.结论来曲唑通过促进异位内膜细胞凋亡来治疗大鼠子宫内膜异位症模型.来曲唑会引起子宫内膜异位症模型大鼠卵巢过度刺激、子宫重量减轻、子宫内膜呈增生抑制状态.

关键词：芳香酶抑制剂/药理学三唑类/药理学子宫内膜异位症/药物疗法泌尿生殖系统/药物作用

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来曲唑对体外培养子宫内膜异位细胞增殖的影响

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中国医师杂志 2009年第6期11卷 859-860页

作者：庞凤飞曹芳蕾浙江省天台县中医院浙江天台317200 辽宁医学院附属第三医院妇产科

目的探讨来曲唑对体外培养的子宫内膜异位症患者在位内膜细胞的增殖影响。方法MTF比色法检测来曲唑对位内膜细胞（EE）／正常内膜（NE）抑制情况，并采用蛋白印迹法与RT—PCR方法检测芳香化酶及其转录调节因子SF-1的蛋白与mRNA表达情况... 详细信息

目的探讨来曲唑对体外培养的子宫内膜异位症患者在位内膜细胞的增殖影响。方法MTF比色法检测来曲唑对位内膜细胞（EE）／正常内膜（NE）抑制情况，并采用蛋白印迹法与RT—PCR方法检测芳香化酶及其转录调节因子SF-1的蛋白与mRNA表达情况。结果NE细胞用药组与对照组比较差异无统计学意义（P〉0．05）；EE细胞在来曲唑作用下呈现较强的抑制增殖效应，其抑制作用随浓度增加而加强，细胞增殖活力明显降低，差异有统计学意义（P〈0．01），不同浓度的来曲唑均可明显抑制细胞内芳香化酶及其转录调节因子SF-1的蛋白与mRNA表达，且呈剂量依赖性，差异有统计学意义（P〈0．01）。结论芳香化酶抑制剂-来曲唑对内异症在位内膜细胞具有抑制其增殖作用，明显抑制EE细胞内芳香化酶及其转录调节因子SF-1的蛋白与mRNA表达。

关键词：三唑类/药理学子宫内膜异位症/药物疗法细胞增彩药物作用

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Synergistic up-regulation of vascular endothelial growth factor expression in murine macrophages by adenosine A_2A receptor agonists and endotoxin

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AMERICAN JOURNAL OF PATHOLOGY 2002年第6期160卷 2231-2244页

作者： Leibovich, SJ Chen, JF Pinhal-Enfield, G Belem, PC Elson, G Rosania, A Ramanathan, M Montesinos, C Jacobson, M Schwarzschild, MA Fink, JS Cronstein, B Univ Med & Dent New Jersey New Jersey Med Sch Dept Cell Biol & Mol Med Newark NJ 07103 USA Massachusetts Gen Hosp Mol Neurobiol Lab Dept Neurol Boston MA 02114 USA Harvard Univ Sch Med Boston MA 02115 USA NYU Sch Med Dept Med New York NY USA NYU Sch Med Div Clin Pharmacol New York NY USA Merck & Co Inc West Point PA USA

Under normoxic conditions, macrophages from C57BL mice produce low levels of vascular endothelial growth factor (VEGF). Hypoxia stimulates VEGF expression by similar to500%;interferon-gamma (IFN-gamma) with endotoxin [lipopolysaccharide (LPS)] also stimulates VEGF expression by similar to50 to 150% in an inducible nitric oxide synthase (iNOS)-dependent manner. Treatment of normoxic macrophages with 5'-N-ethyl-carboxamido-adenosine (NECA), a nonselective adenosine A, receptor agonist, or with 2-[p-(2-carboxyethyl)-phenylethyl amino]-5'-N-ethyl-carboxamido-adenosine (CGS21680), a specific adenosine A(2A) receptor agonist, modestly increases VEGF expression, whereas 2-chloro-N-6-cyclopentyl adenosine (CCPA), an adenosine A(1) agonist, does not. Treatment with LPS (0 to 1000 ng/ml), or with IFN-gamma (0 to 300 U/ml), does not affect VEGF expression. In the presence of LPS (EC50 < 10 ng/ml), but not of IFN-gamma, both NECA and CGS21680 synergistically up-regulate VEGF expression by as much as 10-fold. This VEGF is biologically active in vivo in the rat corneal bioassay of angiogenesis. Inhibitors of iNOS do not affect this synergistic induction of VEGF, and macrophages from iNOS-/- mice produce similar levels of VEGF as wildtype mice, indicating that NO does not play a role in this induction. Under hypoxic conditions, VEGF expression is slightly increased by adenosine receptor agonists but adenosine A(2) or A(1) receptor antagonists 3,7-dimethyl-1-propargyl xanthine (DMPX), ZM241385, and 8-cyclopentyl-1,3-dipropylxanthine (DCPCX) do not modulate VEGF expression. VEGF expression is also not reduced in hypoxic macrophages from A(3)-/- and A(2A)-/- mice. Thus, VEGF expression by hypoxic macrophages does not seem to depend on endogenously released or exogenous adenosine. VEGF expression is strongly up-regulated by LPS/NECA in macrophages from A(3)-/- but not A(2A)-/- mice, confirming the role of adenosine A(2A) receptors in this pathway. LPS with NECA strongly up-regulates V

关键词：腺苷/类似物和衍生物腺苷/药理学腺苷-5'-(N-乙基羧基酰胺)/药理学印迹法蛋白质细胞培养的果蝇蛋白质类内皮生长因子/生物合成脂多糖类/药理学淋巴因子/生物合成巨噬细胞腹膜/药物作用巨噬细胞腹膜/代谢膜糖蛋白类/生理学小鼠近交C3H 小鼠近交C57BL 小鼠基因敲除一氧化氮/生理学一氧化氮合酶/生理学一氧化氮合酶Ⅱ型苯乙胺类/药理学蛋白激酶抑制剂 RNA 信使/代谢受体腺苷A2A 受体细胞表面/生理学受体嘌呤能P1/生理学逆转录聚合酶链反应信号传导可可碱/类似物和衍生物可可碱/药理学 Toll样受体4 Toll样受体三嗪类/药理学三唑类/药理学增量调节血管内皮生长因子A 血管内皮生长因子类黄嘌呤类/药理学动物女(雌)性男(雄)性小鼠

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Assessing perfusion and capillary permeability changes induced by a VEGF inhibitor in human tumor xenografts using macromolecular MR imaging contrast media

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ACADEMIC RADIOLOGY 2002年第Sup2期9卷 S328-S329页

作者： Clément, O Pradel, C Siauve, N Frouin, F Bruneteau, G Kahn, E Frija, G Cuénod, CA Univ Paris 05 Fac Med Necker Enfants Malades Lab Rech Imagerie INSERMU494 F-75015 Paris France

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Ca²⁺ entry mediated by store depletion, S-nitrosylation and TRP3 channels -: Comparison of coupling and function

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第37期275卷 28562-28568页

作者： van Rossum, DB Patterson, RL Ma, HT Gill, DL Univ Maryland Sch Med Dept Biochem & Mol Biol Baltimore MD 21201 USA

The mechanism for coupling between Ca2+ stores and store-operated channels (SOCs) is an important but unresolved question. SOC-mediated Ca2+ entry is complex and may reflect more than one type of channel and coupling mechanism. To assess such possible divergence the function and coupling of SOCs was compared with two other distinct yet related Ca2+ entry mechanisms. SOC coupling in DDT1MF-2 smooth muscle cells was prevented by the permeant inositol 1,4,5-trisphosphate (InsP(3)) receptor blockers, 2-aminoethoxydiphenyl borate (2-APB) and xestospongin C. In contrast, Ca2+ entry induced by S-nitrosylation and potentiated by store depletion (Ma, H-T., Favre, C. J., Patterson, R. L., Stone, M. R., and Gill, D. L. (1999) J. Biol Chem. 274, 35318-35324) was unaffected by 2-APB, suggesting that this entry mechanism is independent of InsP(3) receptors. The cycloalkyl lactamimide, MDL-12,330A (MDL), prevented SOC activation (IC50 10 mu M) and similarly completely blocked S-nitrosylation-mediated Ca2+ entry. Ca2+ entry mediated by the TRP3 channel stably expressed in HEK293 cells was activated by phospholipase C-coupled receptors but independent of Ca2+ store depletion (Ma, B-T., Patterson, R. L., van Rossum, D. B., Birnbaumer, L., Mikoshiba, K., and Gill, D. L. (2000) Science 287, 1647-1651). Receptor-induced TRP3 activation was 2-APB-sensitive and fully blocked by MDL. Direct stimulation of TRP3 channels by the permeant diacylglycerol derivative, 1-oleoyl-2-acetyl-sn-glycerol, was not blocked by 2-APB, but was again prevented by MDL. The results indicate that although the activation and coupling processes for each of the three entry mechanisms are distinct, sensitivity to MDL is a feature shared by all three mechanisms, suggesting there may be a common structural feature in the channels themselves or an associated regulatory component.

关键词：钙/代谢钙通道/生理学仓鼠亚科甘油二酯类/药理学亚胺类/药理学肌醇1 4 5-三磷酸受体受体胞质和核/生理学 TRPC阳离子通道三唑类/药理学动物男(雄)性

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Carboxyamido-triazole inhibits angiogenesis by blocking the calcium-mediated nitric-oxide synthase-vascular endothelial growth factor pathway

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期292卷 31-37页

作者： Bauer, KS Cude, KJ Dixon, SC Kruger, EA Figg, WD NCI Div Clin Sci Med Branch NIH Bethesda MD 20892 USA

The induction of angiogenesis is known to play a critical role in the successful growth, invasion, and metastasis of a tumor. A tumor will not grow beyond a few cubic millimeters without the formation of its own capillary network. Several antiangiogenic agents are under investigation in the clinic setting for the treatment of cancer. Carboxyamido-triazole (CAI), an inhibitor of Ca2+-mediated signal transduction, has been previously shown to inhibit angiogenesis in vitro and in vivo and to downregulate matrix metalloproteinase-2 in vitro. Diminished levels of intracellular Ca2+ result in decreased nitric-oxide synthase (NOS) activity and thereby inhibit the production and release of NO. The antiangiogenic activity of CAI was investigated by assessing microvessel growth from rat aortic segments and in cell culture using human aortic endothelial cells (HAECs). With these models, vascular endothelial growth factor (VEGF) and NOS production and secretion were evaluated. CAI concentrations ranging from 0.25 to 12.0 mu g/ml inhibited new microvessel formation in rat aortic cultures and HAEC proliferation in a dose-dependent manner. Additionally, HAECs treated with CAI showed a dose-dependent decrease of NOS expression and a decrease in both VEGF expression and secretion. Rat aortic segments demonstrated decreased VEGF expression in situ on immunostaining. These data suggest that modulation of the NOS-NO-VEGF pathway through Ca2+-mediated signaling by CAI inhibits angiogenesis in vitro.

关键词：主动脉胸/生理学钙通道阻滞药/药理学细胞分裂/药物作用细胞培养的剂量效应关系药物内皮生长因子/拮抗剂和抑制剂内皮生长因子/代谢内皮血管/药物作用内皮血管/代谢淋巴因子/拮抗剂和抑制剂淋巴因子/代谢微循环/代谢微循环/病理学新生血管化病理性/预防和控制一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢大鼠 Sprague-Dawley 三唑类/药理学血管内皮生长因子A 血管内皮生长因子类动物人类男(雄)性大鼠

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Down-regulation of vascular endothelial growth factor expression after A_2A adenosine receptor activation in PC12 pheochromocytoma cells

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第3期293卷 779-787页

作者： Olah, ME Roudabush, FL Univ Cincinnati Coll Med Dept Pharmacol & Cell Biophys Cincinnati OH 45267 USA

Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen that promotes angiogenesis during embryonic development and the progression of certain pathologies. This study examined the regulation of VEGF expression by adenosine receptor (AR) activation in PC12 rat pheochromocytoma cells. Treatment of cells with the AR agonist CGS21680 reduced the VEGF mRNA level to similar to 20% of that in control cells with an EC50 value of 0.47 nM, indicative of mediation by the A(2A)AR. Downregulation of VEGF mRNA by CGS21680 was abolished by pretreatment of cells with the AR antagonist ZM241385. Additionally, ZM241385 alone increased VEGF mRNA by 2.8-foId above basal. RNase protection assays indicated that CGS21680 down-regulated VEGF(121), VEGF(165), and VEGF(189) transcripts. VEGF protein secretion was similarly decreased by CGS21680. Under hypoxic conditions, VEGF mRNA expression was reduced by 85.7% after pretreatment with CGS21680. The down-regulation response appears to be mediated predominately by coupling of the A(2A)AR to G(s) because cholera toxin treatment also reduced VEGF expression. The decrease in VEGF mRNA steady-state levels after A(2A)AR activation is apparently due to a decrease in the VEGF gene transcription rate and not to a decrease in mRNA stability. Thus, depending on the cell type, adenosine may have an inhibitory effect on VEGF production, which may have implications in blood vessel development.

关键词：腺苷/类似物和衍生物腺苷/药理学减量调节内皮生长因子/遗传学基因表达调控淋巴因子/遗传学 PC12细胞苯乙胺类/药理学 RNA 信使/分析受体嘌呤能P1/生理学信号传导三嗪类/药理学三唑类/药理学血管内皮生长因子A 血管内皮生长因子类动物大鼠

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Fusion genetic analysis of gibberellin signaling mutants

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PLANT JOURNAL 2000年第5期22卷 427-438页

作者： Raventos, D Meier, C Mattsson, O Jensen, AB Mundy, J Inst Mol Biol DK-1353 Copenhagen K Denmark

A fusion genetic strategy was used to identify gibberellin (GA) signaling mutants in transgenic Arabidopsis expressing the beta-glucuronidase (GUS) and firefly luciferase (LUC) reporter genes under control of the GA-responsive GASA1 promoter. Initial analyses determined the spatial and temporal patterns of reporter expression, and showed that reporter induction by GA was antagonized by ABA. gamma-Irradiated M-2 progeny with altered reporter activities were identified by LUC bioimaging followed by GUS assays and northern hybridization of the endogenous GASA1 mRNA. Genetic analysis showed that three mutants, which overexpressed both reporters and endogenous GASA1, were caused by recessive (goe1 and goe2, for GASA over-expressed) and semi-dominant (goe3) mutations at different loci. These mutants are altered in their sensitivity to GA and the GA biosynthetic inhibitor paclobutrazol, and in the expression of several GA signaling related genes.

关键词：碱基序列 DNA引物赤霉素类/遗传学赤霉素类/代谢葡糖醛酸糖苷酶/遗传学萤光素酶类/遗传学发光测定法突变植物生长调节物/药理学植物基因修饰重组融合蛋白质类/遗传学信号传导/遗传学三唑类/药理学

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Selective involvement of reactive oxygen intermediates in platelet-activating factor-mediated activation of NF-κB

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INFLAMMATION 2000年第5期24卷 385-398页

作者： Choi, JH Chung, WJ Han, SJ Lee, HB Choi, IW Lee, HK Jang, KY Lee, DG Han, SS Park, KH Im, SY Chonnam Natl Univ Coll Nat Sci Dept Biol Sci Kwangju 500757 South Korea Chonbuk Natl Univ Sch Med Inst Med Sci Dept Immunol Chonju South Korea Chonbuk Natl Univ Sch Med Inst Med Sci Dept Pathol Chonju South Korea Korea Res Inst Chem Technol Daejon South Korea Chonbuk Natl Univ Dept Biol Educ Chonju South Korea

Although it has been suggested that some biological activities of platelet-activating factor (PAF) are mediated by, at least in part, reactive oxygen intermediates (ROI), the precise mechanisms underlying the interaction between the two remains to be elucidated. Antioxidants, such as ar-tocopherol acid succinate, N-acetyl-L-Cysteine, pyrrolidinedithiocarbamate failed to inhibit PAF-induced immediate systemic reactions such as lethality, symptoms of disseminated intravascular coagulation, and histological changes such as pulmonary edema and hemorrhage in renal medullae 10 min following PAF injection. In contrast, antioxidants significantly inhibited both the in vivo and in vitro PAF-induced NF-kappa B activation and NF-kappa B-dependent TNF-alpha expression. The effects of the antioxidants were due to their inhibition of PAF-induced degradation of I kappa B alpha, a protein responsible for keeping NF-kappa B in an inactive form. A protein tyrosine kinase and N-tosyl-L-phenylalanine chloromethyl ketone sensitive serine protease were involved in both PAF- and H2O2-induced NF-kappa B activation. Collectively, these data indicate that the PAF-induced NF-kappa B activation is selectively mediated through the generation of ROI.

关键词：乙酰半胱氨酸/药理学抗氧化剂/药理学吖庚因类/药理学苯醌类 DNA结合蛋白质类/代谢弥漫性血管内凝血/化学诱导基因表达调控/药物作用染料木黄酮/药理学出血/化学诱导过氧化氢/药理学 I-κB蛋白质类异黄酮类/药理学肾髓质/血液供给内酰胺类大环半数致死量巨噬细胞/药物作用巨噬细胞/代谢小鼠近交C57BL NF-κB/代谢磷酰化血小板活化因子/拮抗剂和抑制剂血小板活化因子/药理学血小板活化因子/毒性蛋白质加工转译后蛋白酪氨酸激酶类/生理学肺水肿/化学诱导吡咯烷类/药理学醌类/药理学活性氧/代谢利福布丁/类似物和衍生物丝氨酸蛋白酶抑制剂/药理学信号传导/药物作用无特异性病原体有机物琥珀酸/药理学硫代氨基甲酸酯类/药理学甲苯磺酰苯丙氨酰氯甲酮/药理学三唑类/药理学肿瘤坏死因子α/生物合成肿瘤坏死因子α/遗传学维生素E/药理学动物女(雌)性小鼠

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In vivo activity of the bis-triazole D0870 against drug-susceptible and drug-resistant strains of the protozoan parasite Trypanosoma cruzi

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JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY 2000年第1期46卷 137-140页

作者： Molina, J Brener, Z Romanha, AJ Urbina, JA Inst Venezolano Invest Cient Ctr Biofis & Bioquim Lab Quim Biol Caracas 1020A Venezuela Cent Univ Venezuela Inst Zool Trop Dept Parasitol Caracas 1041 Venezuela Fundacao Oswaldo Cruz Ctr Pesquisas Rene Rachou Lab Doenca Chagas Belo Horizonte MG Brazil Fundacao Oswaldo Cruz Ctr Pesquisas Rene Rachou Lab Parasitol Celular & Mol Belo Horizonte MG Brazil

We report the in vivo activity of the bis-triazole derivative D0870 against a variety of strains of Trypanosoma cruzi, the causative agent of Chagas' disease, including nitroimidazole/nitrofuran-resistant strains. In both acute and chronic murine models of the disease, treatment with D0870 at greater than or equal to 10 mg/kg on alternate days for a total of 20 doses provided 60-100% protection against death, regardless of the drug sensitivity of the infecting strain. In the acute model we obtained 70-100% parasitological cure in seven of the nine strains tested, including one intermediate and two highly drug-resistant strains. D0870 was able to cure 30-45% of animals chronically infected with various strains, including those harbouring the Colombiana strain, among which no cures were obtained with benznidazole. We also found that the anti-T. cruzi activity of D0870 is largely retained even if the hosts ave immunosuppressed.

关键词： Chagas病/药物疗法 Chagas病/寄生虫学抗药性三唑类/药理学三唑类/治疗应用抗锥虫药/药理学克鲁斯锥虫/药物作用动物女(雌)性小鼠

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