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小鼠Lin28基因的克隆及原核表达

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中国实验动物学报 2011年第6期19卷 456-460页

作者：宁方勇王春生张秋婷安星兰朴善花安铁洙东北林业大学生命科学学院哈尔滨150040 东北农业大学动物科技学院哈尔滨150030

目的探讨获取小鼠Lin28蛋白的方法。方法提取8.5 d ICR小鼠胚胎mRNA后反转录为cDNA序列,用一对两端引入特定酶切位点(NcoⅠ及XhoⅠ)引物,从该cDNA中扩增出Lin28基因编码区序列;将获得的Lin28基因编码区序列克隆到pMD18-T载体上。对质... 详细信息

目的探讨获取小鼠Lin28蛋白的方法。方法提取8.5 d ICR小鼠胚胎mRNA后反转录为cDNA序列,用一对两端引入特定酶切位点(NcoⅠ及XhoⅠ)引物,从该cDNA中扩增出Lin28基因编码区序列;将获得的Lin28基因编码区序列克隆到pMD18-T载体上。对质粒双酶切回收其中Lin28基因片段,与pET-30a(+)载体相连接并转化Rosetta(DE3)型大肠杆菌,用IPTG诱导表达,最后采用SDS-PAGE对表达结果进行分析。结果对所克隆的Lin28蛋白编码区的DNA序列分析表明,Lin28 CDS区包括终止密码子在内为630 bp,与参照DNA(NM_145833)相比同源性为99.37%,与参照氨基酸序列相比同源性为100%;在IPTG诱导下pET-30a(+)-Lin28重组质粒可表达与预期相符的约为27.5×103的蛋白质。结论利用克隆的小鼠Lin28基因,采用原核表达方法,成功获得小鼠Lin28蛋白,为进一步开展以重组蛋白诱导体细胞重编程研究奠定基础。

关键词： ICR小鼠 Lin28 克隆原核表达

8-Hydroxyquinolylnitrones as multifunctional ligands for the therapy of neurodegenerative diseases

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Acta Pharmaceutica Sinica B 2023年第5期13卷 2152-2175页

作者： Damijan Knez Daniel Diez-Iriepa Mourad Chioua Andrea Gottinger Milica Denic Fabien Chantegreil Florian Nachon Xavier Brazzolotto Anna Skrzypczak-Wiercioch Ane Meden Anja Pilar Janko Kos Simon akelj Jure Stojan Kinga Saat Julia Serrano Ana Patricia Fernández Aitana Sánchez-García Ricardo Martínez-Murillo Claudia Binda Francisco López-Muoz Stanislav Gobec JoséMarco-Contelles University of Ljubljana Faculty of PharmacyLjubljana 1000Slovenia Laboratory of Medicinal Chemistry(Institute of Organic Chemistry CSIC)Madrid 28006Spain Departamento de Química Orgánicay Química Inorgánica Alcaláde HenaresMadrid 28871Spain Department of Biology and Biotechnology University of PaviaPavia 27100Italy Département de Toxicologie et Risques Chimiques Institut de Recherche Biomédicale des ArméesParis 91220France Department of Animal Anatomy and Preclinical Sciences University Centre of Veterinary Medicine JU-UAUniversity of Agriculture in KrakowKrakow 30-059Poland Institute of Biochemistry Faculty of MedicineUniversity of LjubljanaLjubljana 1000Slovenia Department of Pharmacodynamics Chair of PharmacodynamicsFaculty of PharmacyJagiellonian University Medical CollegeKrakow 30-688Poland Department of Translational Neurobiology Neurovascular Research GroupCajal Institute(CSIC)Madrid 28002Spain Biotechnology and Vegetal Biology Department Escuela Técnica Superior de Ingeniería AgronómicaAlimentaria y de BiosistemasUniversidad Politécnica de MadridMadrid 28040Spain Faculty of Health Camilo JoséCela University of Madrid(UCJC)Neuropsychopharmacology Unit“Hospital 12 de Octubre”Research InstituteMadrid 28692Spain

We describe the development of quinolylnitrones(QNs)as multifunctional ligands inhibiting cholinesterases(ChEs:acetylcholinesterase and butyrylcholinesterase—h BChE)and monoamine oxidases(hMAO-A/B)for the therapy of neurodegenerative *** identified QN 19,a simple,low molecular weight nitrone,that is readily synthesized from commercially available *** 19 has no typical pharmacophoric element to suggest ChE or MAO inhibition,yet unexpectedly showed potent inhibition of h BChE(IC50=1.06±0.31 nmol/L)and h MAO-B(IC_(50)=4.46±0.18μmol/L).The crystal structures of 19 with hBChE and hMAO-B provided the structural basis for potent binding,which was further studied by enzyme *** 19 acted as a free radical scavenger and biometal chelator,crossed the blood—brain barrier,was not cytotoxic,and showed neuroprotective properties in a 6-hydroxydopamine cell model of Parkinson's *** addition,in vivo studies showed the anti-amnesic effect of 19 in the scopolamine-induced mouse model of AD without adverse effects on motoric function and ***,chronic treatment of double transgenic APPswe-PS1δE9 mice with 19 reduced amyloid plaque load in the hippocampus and cortex of female mice,underscoring the disease-modifying effect of QN 19.

关键词： Quinolylnitrone Butyrylcholinesterase Monoamine oxidase B Alzheimer's disease Multifunctional ligands 6-Hydroxydopamine model Passive avoidance task Novel object recognition

氨氯地平和阿托伐他汀对高血压大鼠血浆及心肌血管紧张肽Ⅱ的影响

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中国新药与临床杂志 2009年第3期28卷 191-195页

作者：鲁静朝崔炜张海林刘德敏杨晓红张冀东刘凡谢瑞芹都军河北医科大学第二医院心内科、河北省心脑血管病研究所河北石家庄050000 河北医科大学药理学教研室河北石家庄050017

目的观察氨氯地平、阿托伐他汀单药和联合用药对自发性高血压大鼠(SHR)循环及心肌血管紧张肽Ⅱ(AngⅡ)的影响,探讨联合用药改善左室肥厚的机制。方法8只雄性Wistar-Kyoto大鼠(WKY大鼠)作为正常血压WKY对照组;雄性SHR32只,随机分为4组,每... 详细信息

目的观察氨氯地平、阿托伐他汀单药和联合用药对自发性高血压大鼠(SHR)循环及心肌血管紧张肽Ⅱ(AngⅡ)的影响,探讨联合用药改善左室肥厚的机制。方法8只雄性Wistar-Kyoto大鼠(WKY大鼠)作为正常血压WKY对照组;雄性SHR32只,随机分为4组,每组8只,即SHR对照组、氨氯地平组(10mg·kg-1·d-1)、阿托伐他汀组(10mg·kg-1·d-1)、联合用药组(氨氯地平10mg·kg-1·d-1及阿托伐他汀10mg·kg-1·d-1)。灌胃给药12wk后,应用形态测量学测定左室质量指数(LVMI),经胸超声心动图测定心室壁厚度、左室重量(LVW)及心脏舒张功能,应用放射免疫法测定大鼠血浆及心肌AngⅡ含量,ELASA法测定血浆BNP含量。结果阿托伐他汀抑制了氨氯地平诱发的循环AngⅡ含量增高[(418±s117)ng·L-1vs(872±128)ng·L-1,P<0.01],降低了心肌AngⅡ含量(P<0.01)。氨氯地平、阿托伐他汀单药及联合用药均明显降低LVMI、血浆BNP含量(均P<0.01),逆转了左室肥厚,这一作用在联合用药时尤为明显(P<0.01)。氨氯地平及阿托伐他汀联合用药明显缩短了SHR的等容舒张时间(IVRT)[(29±4)msvs(40±5)ms,P<0.01]。结论氨氯地平和阿托伐他汀联合用药对高血压左室肥厚及舒张功能的改善具有协同效应,其机制可能与联合用药降低循环及心肌AngⅡ含量有关。

关键词：氨氯地平阿托伐他汀高血压血管紧张肽Ⅱ