Rofecoxib_HNMR_08223_MedChemExpress
南洋楹溃疡病菌巢式PCR快速检测
南洋楹溃疡病菌巢式PCR快速检测作者：敖莉丝王伟任董董李慧静黄嘉琪纪春艳来源：《热带作物学报》2020年第02期摘要：由可可毛色二孢菌（Lasiodiplodia theobromae）引致的潰疡病是目前威胁南洋楹健康生产和品质的重要病害。
快速、准确检测病原菌是进行病害有效防控的基础。
本研究用南洋楹溃疡病菌翻译延伸因子（EF 1-α）编码基因上保守靶基因区域的序列设计特异性引物EF-AF/AR。
利用EF 1-α编码基因通用引物EF-688F/986R和特异性引物EF-AF/AR组合进行巢式PCR扩增，获得264 bp的单一条带，灵敏度检测最低限度为1 fg/µL。
利用建立的巢式PCR方法对林间疑似溃疡病的病样进行检测，能够特异性地检测到L. theobromae。
本研究建立的巢式PCR检测方法准确、特异且灵敏性高，可为南洋楹溃疡病的早期诊断和及时防控提供基础的理论和实践依据。
关键词：南洋楹溃疡病;可可毛色二孢;巢式PCR中图分类号：S432.4 文献标识码：AAbstract： A rapid nested-PCR detection system for Falcataria moluccana stem canker disease was established. The outer pair of primers EF-688F/986R and the inner pair of primers EF-AF/AR were designed based on the EF 1-α gene sequences of Lasiodiplodia t heobromae. The established specific nested-PCR could amplified a single product of 264 bp with annealing temperature of 63℃，reaction cycles of 37. The lowest detectable concentration was 1 fg/µL. L. theobromae could be specifically detected by nested-PCR from the diseased plant samples. The establishment of rapid，sensitive nested-PCR detection system of L. theobromae might have significance in early diagnosis，and disease control of F. moluccana stem canker.Keywords： Falcataria moluccana stem canker; Lasiodiplodia theobromae; nested-PCR南洋楹（Falcataria moluccana）是世界著名的热带速生树种，树形美观，木质纤维丰富，韧性强，材质轻，经营周期短，是家具、造纸制浆等的优良原料。
《溶血磷脂酸对胃癌细胞的增殖迁移作用及其信号通路》范文
《溶血磷脂酸对胃癌细胞的增殖迁移作用及其信号通路》篇一一、引言胃癌是一种常见的消化道恶性肿瘤，其发病率和死亡率均居高不下。
溶血磷脂酸（Lysophosphatidic Acid，LPA）作为一种生物活性脂质，在细胞增殖、迁移等生物学过程中起着重要作用。
近年来，关于LPA在胃癌细胞中的作用及其信号通路的研究逐渐成为热点。
本文旨在探讨溶血磷脂酸对胃癌细胞的增殖迁移作用及其信号通路，以期为胃癌的治疗提供新的思路和方向。
二、溶血磷脂酸的结构与功能溶血磷脂酸是一种重要的生物活性脂质，具有多种生物学功能。
它参与细胞膜的构建和维持，同时也是多种生物活性分子的前体。
在细胞内，LPA通过与细胞膜上的G蛋白偶联受体结合，激活下游信号通路，从而影响细胞的增殖、迁移、分化等生物学过程。
三、溶血磷脂酸对胃癌细胞的作用研究表明，LPA对胃癌细胞的增殖和迁移具有显著的影响。
在胃癌细胞中，LPA能够促进细胞的增殖和迁移，同时抑制细胞的凋亡。
这一过程涉及到多种信号通路的激活，如MAPK、PI3K/AKT等。
这些信号通路的激活进一步促进了胃癌细胞的生长和转移。
四、溶血磷脂酸信号通路的研究LPA对胃癌细胞的增殖迁移作用主要通过激活其信号通路实现。
目前研究认为，LPA主要通过G蛋白偶联受体（GPR）介导的信号通路发挥作用。
在胃癌细胞中，LPA与GPR结合后，激活MAPK、PI3K/AKT等信号分子，进而促进细胞的增殖和迁移。
此外，LPA还可能通过其他信号通路影响胃癌细胞的生物学行为，如Wnt/β-catenin等。
五、信号通路的调控与干预针对LPA信号通路的调控与干预是治疗胃癌的重要策略之一。
目前的研究表明，通过抑制LPA信号通路中的关键分子，如MAPK、PI3K/AKT等，可以抑制胃癌细胞的增殖和迁移。
此外，针对GPR的拮抗剂也可以有效地抑制LPA对胃癌细胞的作用。
这些研究成果为胃癌的治疗提供了新的思路和方向。
六、结论本文探讨了溶血磷脂酸对胃癌细胞的增殖迁移作用及其信号通路。
BFH772_DataSheet_MedChemExpress
Inhibitors, Agonists, Screening Libraries Data SheetBIOLOGICAL ACTIVITY:BFH772 is a potent oral VEGFR2 inhibitor, which is highly effective at targeting VEGFR2 kinase with an IC 50 value of 3 nM.IC50 & Target: IC50: 2.7±0.9 nM (hVEGFR2), 1.5±0.53 μM (mVEGFR2), 1.7±0.36 μM (hVEGFR1), 1.1±0.29 μM (hVEGFR3)[1]In Vitro: BFH772 is highly selective; apart from inhibiting VEGFR2 at 3 nM IC 50, it also targets B–RAF, RET, and TIE–2, albeit with atleast 40–fold lower potency. BFH772 is inactive (IC 50>10 μM; >2 μM for cKIT) against all other tyrosine specific– andserine/threonine–specific protein kinases tested. BFH772 inhibits VEGFR2 with IC 50 of 4.6±0.6 nM in CHO cells. BFH772 inhibits VEGFR2 with IC 50 of 3 nM in HUVEC cells. BFH772 inhibits the ligand induced autophosphorylation of RET, PDGFR, and KIT kinases,with IC 50 values ranging between 30 and 160 nM. BFH772 is selective (IC 50 values >0.5 μM) against the kinases of EGFR, ERBB2,INS–R, and IGF–1R and against the cytoplasmic BCR–ABL kinase. IC 50 of BFH772 (<0.01 nM, n=2) demonstrates that they abrogated VEGF induced proliferation at remarkably low nM concentrations [1].In Vivo: BFH772 at 3 mg/kg orally dosed once per day potently inhibits melanoma growth (by 54–90% for primary tumor and71–96% for metastasis growth) as depicted by treatment to control ratios. Dose–response curves of BFH772 at 0.3, 1, and 3 mg/kg demonstrate that even at the lowest concentrations, this naphthalene–1–carboxamide inhibits VEGF induced tissue weight and TIE–2 levels but only reaches statistical significance at 1 mg/kg and above [1].PROTOCOL (Extracted from published papers and Only for reference)Kinase Assay:[1]In vitro kinase assay is based on a filter binding assay, using the recombinant GST–fused kinase domainsexpressed in baculovirus and purified over glutathione–sepharose, γ–[33P]ATP as the phosphate donor, and poly(Glu:Tyr 4:1) peptide as the acceptor. Each GST–fused kinase is incubated under optimized buffer conditions [20 mM Tris–HCl buffer (pH 7.5), 1–3 mM MnCl 2, 3–10 mM MgCl 2, 3–8 μg/mL poly(Glu:Tyr 4:1), 0.25 mg/mL polyethylene glycol 20000, 8 μM ATP, 10 μM sodium vanadate, 1mM DTT] and 0.2 μCi γ–33P ATP in a total volume of 30 μL in the presence or absence of a test substance for 10 min at ambient temperature. The reaction is stopped by adding 10 mL of 250 mM EDTA. Using a 384–well filter system, half the volume istransferred onto an Immobilon–polyvinylidene difluoride membrane. The membrane is then washed extensively and dried, and scintillation counting is performed. IC 50s for compounds are calculated by linear regression analysis of the percentage inhibition [1].Cell Assay: BFH772 is dissolved in DMSO (10 mM) and stored, and then diluted with appropriate medium before use [1]. [1]DifferentBa/F3 cell lines rendered IL–3 independent by transduction with various constitutively active tyrosine kinases are grown in RPMI 1640 medium containing 10% fetal calf serum. For maintenance of parental Ba/F3 cells, the medium is additionally supplemented with 10 ng/mL interleukin–3 (IL–3). For proliferation assays, Ba/F3 cells are seeded on 96–well plates in triplicates at 10000 cells per well and incubated with various concentrations of compounds for 72 h followed by quantification of viable cells using a resazurin sodium salt dye reduction readout (commercially known as Alamar Blue assay). IC 50s are determined with the XLFit Excel Add–In using a four–parameter dose response model [1].Animal Administration: BFH772 is prepared in PEG200 100% (Mice)[1].Product Name:BFH772Cat. No.:HY-100419CAS No.:890128-81-1Molecular Formula:C 23H 16F 3N 3O 3Molecular Weight:439.39Target:VEGFR Pathway:Protein Tyrosine Kinase/RTK Solubility:DMSO: 7.75 mg/mLBFH772 is dissolved in N–methyl pyrrolidone/polyethylene glycol200 (30:70, v/v) (Rat)[1].[1]Mice[1]Female FVB mice weighing between 18 and 20 g are housed in groups of six. Porous chambers containing VEGF (2 μg/mL) in 0.5 mL of 0.8% w/v agar (containing heparin, 20 U/mL) are implanted subcutaneously in the flank of the mice (n=6 per group). VEGF induces the growth of vascularized tissue around the chamber. This response is dose–dependent and can be quantified by measuring the weight and TIE–2 levels of the tissue. Mice are treated either orally once daily with compounds or vehicle (PEG200 100%, 5 mL/kg) starting4–6 h before implantation of the chambers and continuing for 4 days. The animals are sacrificed for measurement of the vascularized tissues 24 h after the last dose. Tissue weight is taken and then a lysate prepared for TIE–2 ELISA analysis .Rat[1]Catheters are implanted into the femoral artery and vein of na?ve female rats strain OFA for BFH772, and BAW2881, or in the jugular vein and femoral artery in female Sprague–Dawley rats for compounds 4, 9, and 10. Animals are allowed to recover for 96 h and are housed in single cages with free access to food and water throughout the experiment. Female OFA rats received 2.5 mg/kg ofBAW2881 dissolved in ethanol/dimethylisosorbide/polyethylene glycol400/D5W (10/15/35/40 v/v) or 1 mg/kg of BFH772 dissolved in N–methyl pyrrolidone/polyethylene glycol200 (30:70, v/v) via injection into the femoral vein. D5W is glucose 5%/water (v/v). Oral administration: BAW2881 and BFH772 are formulated as a micronized suspension (dissolved/suspended in 0.5% carboxymethyl cellulose in distilled water) and administered by gavage to female OFA rats to deliver a dose of 25 mg/kg for BAW2881 or 3 mg/kg BFH772 (n=4 rats per group). For compounds 4, 9, and 10, female Sprague–Dawley rats at 8 weeks of age received an intraveno References:[1]. Bold G, et al. A Novel Potent Oral Series of VEGFR2 Inhibitors Abrogate Tumor Growth by Inhibiting Angiogenesis. J Med Chem. 2016 Jan 14;59(1):132–46.Caution: Product has not been fully validated for medical applications. For research use only.Tel: 609-228-6898 Fax: 609-228-5909 E-mail: tech@Address: 1 Deer Park Dr, Suite Q, Monmouth Junction, NJ 08852, USA。
过氧化物酶体增殖物激活受体为靶点的非酒精性脂肪肝药物研究进展
过氧化物酶体增殖物激活受体为靶点的非酒精性脂肪肝药物研究进展刘雪（中国海洋大学山东·青岛266003）摘要非酒精性脂肪肝（NAFLD）是肝细胞内脂肪过度沉积的临床病征。
过氧化物酶体增殖物激活受体家族（PPARs）是一种重要的核转录因子，对NAFLD的治疗具有重要的影响。
本文总结了PPARs在NAFLD生理进程中的调节作用和PPARs激动剂在NAFLD治疗中的应用，以期为基于PPARs为靶点的NAFLD药物的设计和开发总结经验。
关键词非酒精性脂肪肝过氧化物酶体增殖物激活受体中图分类号：R282.71文献标识码：A非酒精性脂肪肝(Non-alcohol Fatty Liver Disease，NA-FLD)是指除外酒精和其他明确的损肝因素所致的肝细胞内脂肪过度沉积的临床病征，能够导致一系列严重的肝脏损伤，如非酒精性脂肪肝炎(Non-alcoholic steatohepatitis,NASH)、肝硬化甚至肝癌。
NAFLD的发病机制尚未完全明确，“二次打击”假说认为：脂肪在肝脏的异常积累是首次打击，二次打击则是在首次打击的基础上引发氧化应激，从而引起肝细胞发生炎症甚至纤维化。
由于NAFLD发病机制复杂，因此导致NAFLD 发展的所有因素都是其治疗的潜在靶点，核转录因子是能够与配体结合并调控下游基因转录活性的调节物，在以往的研究中，核转录因子具有治疗NAFLD的潜力。
本文以核转录因子中的过氧物酶体增殖体激活受体（Peroxisome proliferator activated receptors,PPARs）为例，介绍该家族在NAFLD生理进程中的调节作用和PPARs激动剂在NAFLD治疗中的应用。
1PPARs组成与组织表达PPARs属于核受体超家族,包括三个亚型，分别是PPAR、PPAR和PPAR。
PPAR主要在肝脏以及其他代谢活跃的组织中表达，能够上调一系列参与线粒体脂肪酸氧化、微粒体氧化等过程相关酶的活性，因此可以通过加速脂肪酸的氧化减轻肝脏甘油三酯积累。
材料表面浸润性对细菌粘附的影响
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的性也对其抗细菌粘附的 有影响，
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研究论文
材料表面浸润性对细菌粘附的影响
,
,
,
6
(食品科学与技术国家重点实验室，江南大学，江苏无锡214122)
摘要：材料表面的细菌粘附常引起食品腐败或植入性感染，有时甚至会引发疾病，而控制细菌 在材料表面的初始粘附能够减少这些安全隐N。作者通过化学接枝的方法，制备了不同表面浸 润性的材料，并与大肠杆菌、铜绿假单胞菌及金黄色葡萄球菌等3种常见致病菌共同培养,系统 地研究了材料表面浸润性对细菌粘附的影响。研究结果表明，随着材料表面疏水性的增加，其抗 细菌粘附能力显著提升。另夕卜，表面带负电材料的抗菌能力更强。这些结果能够帮助理解细菌在 材料表面粘附的内在机理，同时有助于抗菌材料的设计和制备。 关键词：表面接枝；表面浸润性；抑制细菌粘附；生物膜 中图分类号:TS 206.1 文章编号：1673-1689(2019)03-0026-06 DOI: 10.3969/j.issn. 1673-1689.2019.03.004
要的意义。
生物膜的形成分为5个阶段，可逆接触阶段# 不可逆接触阶段、菌落形成阶段、生物膜成熟阶段
以及生物膜老化脱落阶段叫其中，细菌粘附是生物
AR-A014418_DataSheet_MedChemExpress
Inhibitors, Agonists, Screening Libraries Data SheetBIOLOGICAL ACTIVITY:AR–A014418 is a selective and effective GSK3β inhibitor with an IC 50 value of 104 nM, and has no significant inhibition on 26 other kinases.IC50 & Target: IC50: 104 nM (GSK3β)In Vitro: AR–A014418 inhibits tau phosphorylation at a GSK3–specific site (Ser–396) in 3T3 fibroblasts expressing human four–repeat tau protein with IC 50 of 2.7 μM, and protects cultured N2A cells from death induced by blocking PI3K/PKB pathway. In hippocampal slices, AR–A014418 inhibits neurodegeneration mediated by beta–amyloid peptide [1]. While in NGP and SH–5Y–SY cells,AR–A014418 reduces neuroendocrine markers and suppresses neuroblastoma cell growth [2].In Vivo: In ALS mouse model with the G93A mutant human SOD1, AR–A014418 (0–4 mg/kg, i.p.) delays the onset of symptoms,improves motor activity, slows down disease progression, and postpons the endpoint of the disease [3]. In addition, AR–A014418produces inhibition effect on acetic acid– and formalin–induced nociception in mice by modulating NMDA and metabotropic receptor signaling as well as TNF–α and IL–1β transmission in the spinal cord [4].PROTOCOL (Extracted from published papers and Only for reference)Kinase Assay:[1]The competition experiments are carried out in duplicate with 10 concentrations of the inhibitor inclear–bottomed microtiter plates. The biotinylated peptide substrate, biotin–AAEELDSRAGS(PO3H2)PQL, is added at a final concentration of 2 μM in an assay buffer containing 6 milliunits of recombinant human GSK3 (equal mix of both α and β), 12mM MOPS, pH 7.0, 0.3 mM EDTA, 0.01% β–mercaptoethanol, 0.004% Brij 35, 0.5% glycerol, and 0.5 μg of bovine serumalbumin/25 μL and preincubated for 10–15 min. The reaction is initiated by the addition of 0.04 μCi of [γ–33P]ATP and unlabeled ATP in 50 mM Mg(Ac)2 to a final concentration of 1 μM ATP and assay volume of 25 μL. Blank controls without peptide substrate are used.After incubation for 20 min at room temperature, each reaction is terminated by the addition of 25 μL of stop solution containing 5mM EDTA, 50 μM ATP, 0.1% Triton X–100, and 0.25 mg of streptavidin–coated SPA beads corresponding to appr 35 pmol of binding capacity. After 6 h the radioactivity is determined in a liquid scintillation counter. Inhibition curves are analyzed by non–linear regression using GraphPad Prism.Cell Assay: AR–A014418 is dissolved in DMSO.[1]Cell viability is assessed by calcein/propidium iodide uptake. Calcein AM is taken up and cleaved by esterases present within living cells, yielding yellowish–green fluorescence, whereas PI is only taken up by dead cells,which become orange–red fluorescent. In brief, N2A cells are cultured for 2 days in vitro and then treated with 50 μM LY–294002 in the presence of AR–A014418 or vehicle (DMSO) for 24 h. Subsequently, N2A cells are incubated for 30 min with 2 μM PI and 1 μM calcein–AM. The cultures are then rinsed three times with Hanks' buffered saline solution containing 2 mM CaCl 2, and the cells are visualized by fluorescence microscopy using a Zeiss Axiovert 135 microscope. Three fields (selected at random) are analyzed per well (appr 300 cells/field) in at least three different experiments. Cell death is expressed as percentage of PI–positive cells from the total number of cells. In every experiment, specific cell death is obtained after subtracting the number of dead cells present inProduct Name:AR–A014418Cat. No.:HY-10512CAS No.:487021-52-3Molecular Formula:C 12H 12N 4O 4S Molecular Weight:308.31Target:GSK–3; GSK–3Pathway:Stem Cell/Wnt; PI3K/Akt/mTOR Solubility:10 mM in DMSOvehicle–treated cultures.Animal Administration: AR–A014418 is formulated in normal saline.[3]First, to examine the effects of GSK–3 inhibition on the clinical symptoms, life span, and motor behavior function of ALS, 56 Tg mice are divided into four groups. In each group, 0.5 mL of normal saline is mixed with either 0 μg (control group), 1 μg (group A), 2 μg (group B) or 4 μg (group C) of AR–A014418 per gram of mouse, and injected intraperitoneally into 14 animals per group 5 days a week beginning 60 days after birth. The mice are sacrificed at the endpoint described below.References:[1]. Bhat R, Xue Y, Berg S, Structural insights and biological effects of glycogen synthase kinase 3–specific inhibitor AR–A014418. J Biol Chem. 2003 Nov 14; 278(46):45937–45.[2]. Carter YM, et al. Specific glycogen synthase kinase–3 inhibition reduces neuroendocrine markers and suppresses neuroblastoma cell growth. Cancer Biol Ther. 2014 May;15(5):510–5.[3]. Koh SH, et al. Inhibition of glycogen synthase kinase–3 suppresses the onset of symptoms and disease progression of G93A–SOD1 mouse model of ALS. Exp Neurol. 2007 Jun;205(2):336–46.[4]. Martins DF, et al. The antinociceptive effects of AR–A014418, a selective inhibitor of glycogen synthase kinase–3 beta, in mice. J Pain. 2011 Mar;12(3):315–22.Caution: Product has not been fully validated for medical applications. For research use only.Tel: 609-228-6898 Fax: 609-228-5909 E-mail: tech@Address: 1 Deer Park Dr, Suite Q, Monmouth Junction, NJ 08852, USA。
低剂量普通肝素用于ECMO辅助支持患者抗凝治疗的系统评价
•临床评价-低剂量普通肝素用于ECMO辅助支持患者抗凝治疗的系统评价黄晓嫡，赵红卫，马永成，杜鹏强，倪铭，王爱凤(阜外华中心血管病医院药学部，河南郑州450000)［摘要］目的：系统评价低剂量普通肝素(UFH)用于体外膜肺氧合(ECMO)辅助支持患者的抗凝治疗。
方法：计算机检索PubMed、EMbase、Cochrane Library、CNKI、维普、万方和CBM数据库，纳入低剂量UFH用于ECMO辅助支持患者抗凝的回顾性队列研究。
根据NOS量表对纳入研究的质量进行评价。
采用RevMan5.3软件进行Meta分析。
结果：共计纳入5篇文献，包括469例患者，试验组(UFH低剂量)215例，对照组(UFH常规剂量)254例。
NOS评分为7~9分。
Meta分析结果显示，试验组和对照组的ECMO血管插管部位出血发生率分别为15.22%和40.74%,胃肠出血发生率分别为7.32%和14.62%,差异均有统计学意义(P<0.05);与对照组相比，试验组的压缩红细胞(PRBC)平均输注单位显著减少(P<0.01)o两组的手术部位出血、肺出血、颅内出血、血栓形成、ECMO撤机以及在院死亡率均无统计学差异(P>0.05)□结论：对于ECMO辅助支持患者，UFH调低剂量可减少ECMO血管插管部位和胃肠等部分出血事件，降低PRBC平均输注单位。
且尚无证据表明，调低UFH剂量会增加患者的血栓形成，延缓ECMO撤机，甚至提高在院死亡率。
受纳入研究质量及数量的限制，研究结果仍需更多大样本、高质量的研究加以验证。
［关键词］普通肝素；低剂量；体外膜肺氧合；抗凝；系统评价［中图分类号］R973+.2［文献标识码］A［文章编号］1672-8157(2020)06-0355-05Systematic review of the anticoagulant regimen of low-dose unfractioned heparin for patients on ECMOHUANG Xiao-jing,ZHAO Hong-wei,MA Yong-cheng,DU Peng-qiang,NI Ming,WANG A.i-feng(pepartment of Pharmacy,Fuwai Central China Cardiovascular Hospital,Zhengzhou450000,China)[ABSTRACT]Objective:To systematically review the anticoagulant regimen of low-dose unfractioned heparin(UFH)for patients on extracorporeal membrane oxygenation(ECMO).Methods:Databases including PubMed,EMbase,Cochrane Library, CNKI,VH\Wanfang and CBMdisc were searched for retrospective cohort studies about low-dose UFH used for patients on ECMO. Newcastle-Ottawa Scale(NOS)was used to evaluate the quality of the included studies.Meta-analysis was conducted by RevMan 5.3software.Results：A total of5cohort studies with a NOS score of7-9and469patients were included.There were215patients in experimental group(low-dose of UFH)and254patients in control group(routine dose of UFH).Results of meta-analysis showed that the rates of ECMO cannula site bleeding in experimental group and control group were15.22%and40.74%respectively,rates of gastrointestmal bleeding in the two groups were7.32%and14.62%respectively.There were significant dififerences between them(P <0.05).Compared with the control group,mean transfusion units of packed red blood cell(PRBC)markedly declined(P<0.01) in experimental group.Meanwhile,there were no statistical differences in rates of surgical site bleeding,pulmonary bleeding,cerebral bleeding,thrombosis,weaning of ECMO and in-hospital mortality between the two groups(P>0.05).Conclusion：For the patients on ECMO,low-dose UFH might help reduce the rates of cannula site bleeding,gastrointestinal bleeding,mean transfusion units of PRBC and had no influences on thrombosis,weaning of ECMO and the in-hospital mortality,which should be further proved by more studies with high quality due to the limitation of the quality and quantity of cohort studies involved in this study.[KEY WORDS]Unfractioned heparin;Low dose;Extracorporeal membrane oxygenation;Anticoagulation;Systematic review体外膜肺氧合(extracorporeal membrane［基金项目］吴阶平医学基金会临床药学专项基金(3206750190904)［通信作者］王爱凤，女，主任药师，研究方向：医院药学。
Erythrosin_B_SDS_MedChemExpress
Inhibitors, Agonists, Screening LibrariesSafety Data Sheet Revision Date:Jan.-22-2018Print Date:Jan.-22-20181. PRODUCT AND COMPANY IDENTIFICATION1.1 Product identifierProduct name :Erythrosin BCatalog No. :HY-D0259CAS No. :16423-68-01.2 Relevant identified uses of the substance or mixture and uses advised againstIdentified uses :Laboratory chemicals, manufacture of substances.1.3 Details of the supplier of the safety data sheetCompany:MedChemExpress USATel:609-228-6898Fax:609-228-5909E-mail:sales@1.4 Emergency telephone numberEmergency Phone #:609-228-68982. HAZARDS IDENTIFICATION2.1 Classification of the substance or mixtureGHS Classification in accordance with 29 CFR 1910 (OSHA HCS)Acute toxicity, Oral (Category 4), H302Chronic aquatic toxicity (Category 4), H4132.2 GHS Label elements, including precautionary statementsPictogramSignal word WarningHazard statement(s)H302 Harmful if swallowed.H413 May cause long lasting harmful effects to aquatic life.Precautionary statement(s)P264 Wash skin thoroughly after handling.P270 Do not eat, drink or smoke when using this product.P273 Avoid release to the environment.P301 + P312 + P330 IF SWALLOWED: Call a POISON CENTER ⁄doctor if you feel unwell.Rinse mouth.P501 Dispose of contents ⁄ container to an approved waste disposal plant.H413 May cause long lasting harmful effects to aquatic life.2.3 Other hazardsNone.3. COMPOSITION/INFORMATION ON INGREDIENTS3.1 SubstancesSynonyms:Erythrosin extra bluishFormula:C20H6I4Na2O5Molecular Weight:879.86CAS No. :16423-68-04. FIRST AID MEASURES4.1 Description of first aid measuresEye contactRemove any contact lenses, locate eye-wash station, and flush eyes immediately with large amounts of water. Separate eyelids with fingers to ensure adequate flushing. Promptly call a physician.Skin contactRinse skin thoroughly with large amounts of water. Remove contaminated clothing and shoes and call a physician.InhalationImmediately relocate self or casualty to fresh air. If breathing is difficult, give cardiopulmonary resuscitation (CPR). Avoid mouth-to-mouth resuscitation.IngestionWash out mouth with water; Do NOT induce vomiting; call a physician.4.2 Most important symptoms and effects, both acute and delayedThe most important known symptoms and effects are described in the labelling (see section 2.2).4.3 Indication of any immediate medical attention and special treatment neededTreat symptomatically.5. FIRE FIGHTING MEASURES5.1 Extinguishing mediaSuitable extinguishing mediaUse water spray, dry chemical, foam, and carbon dioxide fire extinguisher.5.2 Special hazards arising from the substance or mixtureDuring combustion, may emit irritant fumes.5.3 Advice for firefightersWear self-contained breathing apparatus and protective clothing.6. ACCIDENTAL RELEASE MEASURES6.1 Personal precautions, protective equipment and emergency proceduresUse full personal protective equipment. Avoid breathing vapors, mist, dust or gas. Ensure adequate ventilation. Evacuate personnel to safe areas.Refer to protective measures listed in sections 8.6.2 Environmental precautionsTry to prevent further leakage or spillage. Keep the product away from drains or water courses.6.3 Methods and materials for containment and cleaning upAbsorb solutions with finely-powdered liquid-binding material (diatomite, universal binders); Decontaminate surfaces and equipment by scrubbing with alcohol; Dispose of contaminated material according to Section 13.7. HANDLING AND STORAGE7.1 Precautions for safe handlingAvoid inhalation, contact with eyes and skin. Avoid dust and aerosol formation. Use only in areas with appropriate exhaust ventilation.7.2 Conditions for safe storage, including any incompatibilitiesKeep container tightly sealed in cool, well-ventilated area. Keep away from direct sunlight and sources of ignition.Recommended storage temperature:Powder-20°C 3 years4°C 2 yearsIn solvent-80°C 6 months-20°C 1 monthShipping at room temperature if less than 2 weeks.7.3 Specific end use(s)No data available.8. EXPOSURE CONTROLS/PERSONAL PROTECTION8.1 Control parametersComponents with workplace control parametersThis product contains no substances with occupational exposure limit values.8.2 Exposure controlsEngineering controlsEnsure adequate ventilation. Provide accessible safety shower and eye wash station.Personal protective equipmentEye protection Safety goggles with side-shields.Hand protection Protective gloves.Skin and body protection Impervious clothing.Respiratory protection Suitable respirator.Environmental exposure controls Keep the product away from drains, water courses or the soil. Cleanspillages in a safe way as soon as possible.9. PHYSICAL AND CHEMICAL PROPERTIES9.1 Information on basic physical and chemical propertiesAppearance Pink to red (Solid)Odor No data availableOdor threshold No data availablepH No data availableMelting/freezing point No data availableBoiling point/range No data availableFlash point No data availableEvaporation rate No data availableFlammability (solid, gas)No data availableUpper/lower flammability or explosive limits No data availableVapor pressure No data availableVapor density No data availableRelative density No data availableWater Solubility No data availablePartition coefficient No data availableAuto-ignition temperature No data availableDecomposition temperature No data availableViscosity No data availableExplosive properties No data availableOxidizing properties No data available9.2 Other safety informationNo data available.10. STABILITY AND REACTIVITY10.1 ReactivityNo data available.10.2 Chemical stabilityStable under recommended storage conditions.10.3 Possibility of hazardous reactionsNo data available.10.4 Conditions to avoidNo data available.10.5 Incompatible materialsStrong acids/alkalis, strong oxidising/reducing agents.10.6 Hazardous decomposition productsUnder fire conditions, may decompose and emit toxic fumes.Other decomposition products - no data available.11.TOXICOLOGICAL INFORMATION11.1 Information on toxicological effectsAcute toxicityClassified based on available data. For more details, see section 2Skin corrosion/irritationClassified based on available data. For more details, see section 2Serious eye damage/irritationClassified based on available data. For more details, see section 2Respiratory or skin sensitizationClassified based on available data. For more details, see section 2Germ cell mutagenicityClassified based on available data. For more details, see section 2CarcinogenicityIARC: No component of this product present at a level equal to or greater than 0.1% is identified as probable, possible or confirmed human carcinogen by IARC.ACGIH: No component of this product present at a level equal to or greater than 0.1% is identified as a potential or confirmed carcinogen by ACGIH.NTP: No component of this product present at a level equal to or greater than 0.1% is identified as a anticipated or confirmed carcinogen by NTP.OSHA: No component of this product present at a level equal to or greater than 0.1% is identified as a potential or confirmed carcinogen by OSHA.Reproductive toxicityClassified based on available data. For more details, see section 2Specific target organ toxicity - single exposureClassified based on available data. For more details, see section 2Specific target organ toxicity - repeated exposureClassified based on available data. For more details, see section 2Aspiration hazardClassified based on available data. For more details, see section 212. ECOLOGICAL INFORMATION12.1 ToxicityNo data available.12.2 Persistence and degradabilityNo data available.12.3 Bioaccumlative potentialNo data available.12.4 Mobility in soilNo data available.12.5 Results of PBT and vPvB assessmentPBT/vPvB assessment unavailable as chemical safety assessment not required or not conducted.12.6 Other adverse effectsNo data available.13. DISPOSAL CONSIDERATIONS13.1 Waste treatment methodsProductDispose substance in accordance with prevailing country, federal, state and local regulations.Contaminated packagingConduct recycling or disposal in accordance with prevailing country, federal, state and local regulations.14. TRANSPORT INFORMATIONDOT (US)This substance is considered to be non-hazardous for transport.IMDGThis substance is considered to be non-hazardous for transport.IATAThis substance is considered to be non-hazardous for transport.15. REGULATORY INFORMATIONSARA 302 Components:No chemicals in this material are subject to the reporting requirements of SARA Title III, Section 302.SARA 313 Components:This material does not contain any chemical components with known CAS numbers that exceed the threshold (De Minimis) reporting levels established by SARA Title III, Section 313.SARA 311/312 Hazards:No SARA Hazards.Massachusetts Right To Know Components:No components are subject to the Massachusetts Right to Know Act.Pennsylvania Right To Know Components:No components are subject to the Pennsylvania Right to Know Act.New Jersey Right To Know Components:No components are subject to the New Jersey Right to Know Act.California Prop. 65 Components:This product does not contain any chemicals known to State of California to cause cancer, birth defects, or anyother reproductive harm.16. OTHER INFORMATIONCopyright 2017 MedChemExpress. The above information is correct to the best of our present knowledge but does not purport to be all inclusive and should be used only as a guide. The product is for research use only and for experienced personnel. It must only be handled by suitably qualified experienced scientists in appropriately equipped and authorized facilities. The burden of safe use of this material rests entirely with the user. MedChemExpress disclaims all liability for any damage resulting from handling or from contact with this product.Caution: Product has not been fully validated for medical applications. For research use only.Tel: 609-228-6898 Fax: 609-228-5909 E-mail: tech@Address: 1 Deer Park Dr, Suite Q, Monmouth Junction, NJ 08852, USA。
Keap1
非小细胞肺癌(non-small cell lung cancer，NSCLC)发病率占据肺癌的75%~80%。
肿瘤细胞进展快且易扩散转移，临床常采用手术、放化疗等进行治疗，但5年生存率低于60%[1-2]。
氧化应激是由活性氧(ROS)生成量增加所致，ROS积累可诱导肺癌细胞凋亡，清除ROS 可阻止癌细胞凋亡，即肺癌细胞存活依赖于癌细胞自身抗氧化能力[3]。
Kelch样环氧氯丙烷相关蛋白-1 (kelch-like epichlorohydrin-associated protein-1，Keap1)/核因子E2相关因子2(nuclear factor E2related factor 2，Nrf2)信号通路在癌症中发挥重要调控作用，氧化应激可激活Keap1，促使Keap1-Nrf2复合物裂解，Nrf2转移至细胞核内，可激活下游靶基因表达，参与肺癌发生发展过程[4]。
Nrf2可维持氧化还原稳态，ROS侵袭细胞时，Nrf2可进入细胞核，结合抗氧化反应元件(ARE)转录编码各种抗氧化蛋白、代谢酶基因，抑制氧化应激反应[5-6]。
目前氧化应激、Keap1/Nrf2信号通路在NSCLC发生过程中的机制尚未明确。
基于此，本研究尝试分析Keap1/Nrf2信号通路与临床病理参数、氧化应激指标的相关性，探讨其在NSCLC氧化应激机制中的作用，为临床研制新药提供参考依据。
1资料与方法1.1一般资料选取2017年4月至2020年4月郑州市第三人民医院收治的100例NSCLC患者为研究对象。
纳入标准：符合NSCLC诊断标准[7]；术前未接受放化疗、免疫治疗者；预计生存期≥6个月；符合手术适应证、禁忌证；Karnofsky功能状态评分≥70分；签署知情同意书。
排除标准：合并凝血功能障碍、肝肾功能障碍、其他恶性肿瘤者；伴有急/慢性感染者；伴有精神疾病者；既往腹部相关外科手术史者。
所有患者均行肺癌根治性切除术，术中收集癌组织、癌旁组织(距离癌组织5cm范围内正常组织)，其中男性63例，女性37例；年龄46~67岁，平均(56.32±3.16)岁；体质量指数(BMI)17~30kg/m2，平均(23.16±2.03)kg/m2；病理类型：鳞癌58例、腺癌42例；病理分级[8]：Ⅰ~Ⅱ级51例、Ⅲ级49例；T分期[9]：T1~T253例、T3~T447例；N分期：N055例、N1~N245例。
15523666_迷迭香酸对哮喘小鼠氧化性肺损伤的保护作用
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%!3广西大学动物科学技术学院"南宁 4:8884*"3广西畜牧研究所"南宁 4:888!'
摘要为评价迷迭香酸对哮 喘 小 鼠 模 型 氧 化 性 肺 损 伤 的 保 护 作 用"本 研 究 用 卵 清 蛋 白 %,(;'致 敏$激 发 雌 性 &;B&&S小鼠建立哮喘模型"并用 ,(; 和 Z"," 联合激发小鼠作为氧化肺损伤阳性对照模型#在最后一次滴鼻激 发 "$O 后 "取 支 气 管 肺 泡 灌 洗 液 %&;B['进 行 细 胞 计 数 并 测 定 活 性 氧 %9,D'$超 氧 化 物 歧 化 酶 %D,''和 谷 胱 甘 肽 过 氧化物酶%1DZ?CQ'水平"取左侧肺脏固定做 Z= 染色#结果显示"迷迭香酸可明显减少 &;B[ 中 细 胞 总 数 和 嗜 酸 性粒细胞数目"显著抑制肺组织和 &;B[ 中 9,D的产生"升高 D,' 和 1DZ?CQ水 平"改 善 肺 组 织 病 理 变 化# 本 试 验 结 果 表 明 "迷 迭 香 酸 对 氧 化 肺 损 伤 起 到 明 显 的 保 护 作 用 # 关 键 词 迷 迭 香 酸 *哮 喘 *氧 化 性 肺 损 伤 *抗 氧 化 中 图 分 类 号 9"0434 文 献 标 识 码 ; 文 章 编 号 !+6!?6":+%"8!6'!"?:+48?8+
Rofecoxib_DataSheet_MedChemExpress
Inhibitors, Agonists, Screening Libraries Data SheetBIOLOGICAL ACTIVITY:Rofecoxib(MK 966) is a potent inhibitor of the COX–2–dependent production of PGE2 in human osteosarcoma cells (IC50= 26±10 nM)and Chinese hamster ovary cells expressing human COX–2 (IC50=18±7 nM).IC50 value: 26 nM (cell assay)Target: COX2Rofecoxib is a synthetic, nonsteroidal derivative of phenyl–furanone with antiinflammatory, antipyretic and analgesic properties and potential antineoplastic properties. Rofecoxib binds to and inhibits the enzyme cyclooxygenase–2 (COX–2), resulting in an inhibition of the conversion of arachidonic acid to prostaglandins. COX–related metabolic pathways may represent key regulators of cellproliferation and neo–angiogenesis. Some epithelial tumor cell types overexpress pro–angiogenic COX–2. Rofecoxib was used as an anti–inflammatory analgesic which has now been withdrawn from the market because of its association with cardiovascular problems.PROTOCOL (Extracted from published papers and Only for reference)Cell assay [1]Stably transfected CHO cells expressing human COX–1 and COX–2 were cultured and assayed for the production of PGE2 after stimulation by arachidonic acid as described previously (Kargman et al., 1996). Cells (0.3 × 106 cells in 200 μl) were preincubated in HBSS containing 15 mM HEPES, pH 7.4, with 3 μl of the test drug or DMSO vehicle for 15 min at 37°C before challenge with arachidonic acid. Cells were challenged for 15 min with an arachidonic acid solution [10% ethanol (v/v) in HBSS] to yield finalconcentrations of 10 μM arachidonic acid in the CHO[COX–2] assay and of 0.5 μM arachidonic acid in the CHO[COX–1] assay. In the absence of addition of exogenous arachidonic acid, levels of PGE2 in samples from CHO[COX–1] were <30 pg PGE2/106 cells. In the presence of 0.5 μM exogenous arachidonic acid, levels of PGE2 in samples from CHO[COX–1] cells increased to 260 to 1500 pgPGE2/106cells. After stimulation with 10 μM exogenous arachidonic acid, levels of PGE2 in samples from CHO[COX–2] cells increased from <120 to 700 to 1600 pg PGE2/106 cells. Rofecoxib was typically tested at eight concentrations in duplicate using 3–fold serial dilutions in DMSO. COX activity in the absence of Rofecoxib is determined as the difference in PGE2 levels of cells challenged with arachidonic acid versus the PGE2 levels in cells mock–challenged with ethanol vehicle.Animal administration [1]AIA was induced in six groups of 10 rats (female Lewis, 144–172 g, 7 weeks old), each by an intradermal injection of 0.5 mg ofMycobacterium butyricum in light mineral oil in the left hind foot pad as described previously (Fletcher et al., 1998). Ten rats were not injected and served as nonadjuvant controls. Body weights, radiographs, and foot volumes of the noninjected (secondary) paws were determined on various days (0, 14, and 21). Rofecoxib (0.1, 0.3, 1.0, and 3.0 mg/kg/day p.o.; 0.05, 0.15, 0.5, and 1.5 mg/kg b.i.d.),indomethacin (1 mg/kg/day p.o.; 0.5 mg/kg b.i.d.), and appropriate vehicles were started on day 0 and continued throughout the experiment. Rats were euthanized by carbon dioxide inhalation on day 21. The thymus and spleen of all rats were removed andweighed. To assess tibiotarsal joint integrity, radiographic scores were assigned according to an adaptation of a previously describedProduct Name:Rofecoxib Cat. No.:HY-17372CAS No.:162011-90-7Molecular Formula:C 17H 14O 4S Molecular Weight:314.36Target:COX Pathway:Immunology/Inflammation Solubility:10 mM in DMSOmethod (Clark et al., 1979) by a radiologist who was blinded to treatment. Two–factor (“treatment” and “time”) ANOVA with repeated measures on “time” were applied to the percent changes for body weight and foot volumes and to the rank–transformed radiographic total scores. A post hoc Dunnett’s test was conducted to compare the effect of treatments to vehicle. A one–way ANOVA was applied to the thymic and spleen weights, followed by the Dunnett’s test, to compare the effect of treatments to vehicle.Enzyme assay [1]Rofecoxib was incubated at concentrations ranging from 0.7 to 20μM with partially purified 15–lipoxygenase from human leukocytes in 0.05 M sodium phosphate, pH 6.3, 24 μg/ml phosphatidylcholine, and 20 μM arachidonic acid. After a 10–min incubation at room temperature, the reaction was quenched with acetonitrile and analyzed by reverse phase–HPLC on a C18 column eluted with acetonitrile/water/trifluoroacetic (60:40:0.1) for the quantification of 15–hydroperoxyeicosatetraenoic acid.References:[1]. Chan CC, Boyce S, Brideau C et al. Rofecoxib [Vioxx, MK–0966; 4–(4'–methylsulfonylphenyl)–3–phenyl–2–(5H)–furanone]: a potent and orally active cyclooxygenase–2 inhibitor. Pharmacological and biochemical profiles. J Pharmacol Exp Ther. 1999 Aug;290(2):551–60.[2]. Hillson JL, Furst DE. Rofecoxib. Expert Opin Pharmacother. 2000 Jul;1(5):1053–66.[3]. Weir MR, Sperling RS, Reicin A, Gertz BJ. et al. Selective COX–2 inhibition and cardiovascular effects: a review of the rofecoxib development program. Am Heart J. 2003 Oct;146(4):591–604.[4]. Sun SX, Lee KY, Bertram CT, Goldstein JL. Withdrawal of COX–2 selective inhibitors rofecoxib and valdecoxib: impact on NSAID and gastroprotective drug prescribing and utilization. Curr Med Res Opin. 2007 Aug;23(8):1859–66.Caution: Product has not been fully validated for medical applications. For research use only.Tel: 609-228-6898 Fax: 609-228-5909 E-mail: tech@Address: 1 Deer Park Dr, Suite Q, Monmouth Junction, NJ 08852, USA。
治疗骨关节炎药—Rofecoxib
治疗骨关节炎药—Rofecoxib
朱晓红
【期刊名称】《国外新药介绍》
【年(卷),期】2000(000)004
【总页数】6页(P14-19)
【作者】朱晓红
【作者单位】无
【正文语种】中文
【中图分类】R684.305
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药品中诺氟沙星的量子点荧光猝灭测定法
药品中诺氟沙星的量子点荧光猝灭测定法张媛;谢海婷;高强;李满秀【摘要】目的建立药品中诺氟沙星的量子点荧光猝灭测定法.方法在诺氟沙星溶液中加入适量CdTe量子点溶液和N-羟基丁二酰亚胺(NHS)溶液,用pH=7.5硼砂缓冲溶液定容.混合均匀后在室温下反应30min,测定其荧光强度.结果诺氟沙星在1.9 l～35.09μg/mL范围与体系的F0/F呈良好的线性关系,相关系数r=0.9961,检出限为1.70μg/mL,平均回收率为93.52％～98.75％,RSD为1.1％～4.8％.结论方法具有快速简便,灵敏度和精密度较高的优点,适用于药品中诺氟沙星的检测.【期刊名称】《中国抗生素杂志》【年(卷),期】2016(041)002【总页数】3页(P125-127)【关键词】CdTe量子点;诺氟沙星;NHS;荧光猝灭【作者】张媛;谢海婷;高强;李满秀【作者单位】忻州师范学院化学系,忻州034000;忻州师范学院化学系,忻州034000;忻州师范学院化学系,忻州034000;忻州师范学院化学系,忻州034000【正文语种】中文【中图分类】R978.1诺氟沙星为第三代喹诺酮类抗菌药，具有抗菌谱广、抗菌活性强的特点，在临床上有广泛的应用。
目前，用于诺氟沙星药物的测定方法主要有高效液相色谱法(HPLC)[1-2]，液相色谱-质谱法(LC-MS)[3]、荧光法[4]、紫外光度法[5]等。
量子点[6](QDs)是一种新型半导体荧光纳米材料，近年来在生物显像及诊断、分子生物探针、药物筛选、生物大分子相互作用等方面显示出极大的应用前景[7]，同时基于其荧光增强和猝灭效应，量子点还用于重金属离子[8-9]的检测和药物[10-11]含量的测定。
文献检索未发现利用CdTe量子点与N-羟基丁二酰亚胺(NHS)连接检测诺氟沙星的报道，本文在水相合成了以巯基乙酸为稳定剂的CdTe量子点，利用其与NHS连接后作为荧光探针，进而与诺氟沙星相互作用，使得体系的荧光发生猝灭，从而达到对诺氟沙星检测的目的。