DUBs-IN-1_LCMS_12024_MedChemExpress
MK2-IN-1_hydrochloride_SDS_MedChemExpress
Inhibitors, Agonists, Screening LibrariesSafety Data Sheet Revision Date:Jul.-24-2017Print Date:Jul.-24-20171. PRODUCT AND COMPANY IDENTIFICATION1.1 Product identifierProduct name :MK2-IN-1 (hydrochloride)Catalog No. :HY-12834ACAS No. :1314118-94-91.2 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 mixtureNot a hazardous substance or mixture.2.2 GHS Label elements, including precautionary statementsNot a hazardous substance or mixture.2.3 Other hazardsNone.3. COMPOSITION/INFORMATION ON INGREDIENTS3.1 SubstancesSynonyms:MK2 InhibitorFormula:C27H26Cl2N4O2Molecular Weight:509.43CAS No. :1314118-94-94. 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。
HSF1A_DataSheet_MedChemExpress
Inhibitors, Agonists, Screening Libraries Data SheetBIOLOGICAL ACTIVITY:HSF1A is a cell–permeable activator of heat shock transcription factor 1 (HSF1).IC50 & Target: HSF1[1]In Vitro: HSF1A protects cells from stress–induced apoptosis, binds TRiC subunits and inhibits TRiC activity without perturbation of ATP hydrolysis. Genetic inactivation or depletion of the TRiC complex results in human HSF1 activation and HSF1A inhibits the direct interaction between purified TRiC and HSF1 in vitro. Moreover, fluorescence anisotropy experiments using FITC coupled to HSF1A demonstrates that HSF1A–FITC binds to a purified Tcp1 subunit of TRiC with an affinity of approximately 600 nM. This is validated qualitatively via titration of purified Tcp1 into binding reactions containing 500 nM Biotin or HSF1A–Biotin [1]. Quantification bycounting the number of cell containing aggregates as a function of the total number of cells reveals that at HSF1A concentrations as low as 2 μM, a reduced number of aggregate–containing cells are observed. The fraction of cells containing aggregates continued to decrease in a dose–dependent manner such that pretreatment with 12 μM HSF1A resulta in ~20% of the cells exhibiting aggregates visible by fluorescence microscopy [2].In Vivo: HSF1A enhances HSF1 activity, stabilizes HSF1 expression and minimizes Doxorubicin (DOX)–induced cardiac damage. WKY rats are challenged with DOX (accumulated dose: 30 mg/kgw), and DOX combined with HSF1A (100 mg/kgw/day). Supplementation with HSF1A significantly elevates cardiac functions back to the levels of the control group. HSF1A has been shown to stimulate human HSF1 nuclear translocation, elevate protein chaperone expression and ameliorate protein misfolding and cell death in aneurodegenerative disease model. The echocardiographic results show that HSF1A also alleviates DOX–induced failures in cardiac function [3].PROTOCOL (Extracted from published papers and Only for reference)Kinase Assay:[1]Protein extracts are generated from mammalian, yeast and E. coli cultures using biotin–binding buffer (20 mM HEPES,5 mM MgCl 2, 1 mM EDTA, 100 mM KCl, 0.03% NP–40) supplemented with 1% Trition–X100 and protease inhibitors. Approximately 0.5mg of protein extract is incubated with 100 μM HSF1A–Biotin for 4 h at 4°C and HSF1A–Biotin associated proteins captured by with NeutrAvidin Agarose Resin. After washing in biotin binding buffer proteins are eluted using 50 μL biotin elution buffer (100 mM Tris,150 mM NaCl, 0.1 mM EDTA, 2 mM D–biotin), resolved on a 4–20% SDS–PAGE, and immunoblotted. For purified TRiC and Hsp70analyses, 5 nM protein is incubated in biotin–binding buffer+0.5% Triton X–100 with 100 μM biotin or 100 μM HSF1A–Biotin for 4 h at 4°C and captured with NeutrAvidin Resin. For NiNTA purified yeast Tcp1, different concentrations of Tcp1 0.5 μM, 1 mM, 2 mM, 3 mM and 4 mM in 25 mM Hepes pH 7.5, 150 mM NaCl are incubated with 0.5 μM Biotin or HSF1A–Biotin for 4 h at 4°C and captured with NeutrAvidin Resin [1].Cell Assay:[2]PC12 cells seeded into a 96–well plate (5×104 cells/well) are treated with increasing concentrations of HSF1A (2, 4, 8 andProduct Name:HSF1A Cat. No.:HY-103000CAS No.:1196723-93-9Molecular Formula:C21H19N3O2S2Molecular Weight:409.52Target:HSP Pathway:Cell Cycle/DNA Damage; Metabolic Enzyme/Protease Solubility:DMSO: ≥ 150 mg/mL12 μM) for 15 h, at which time httQ74–GFP expression is stimulated by incubation in the presence of 1 μg/mL Doxycycline for 5 d. Cell viability is assessed via the XTT viability assay[2].Animal Administration:[3]Rat[3]Ten–week–old Wistar Kyoto rats (WKY) are used. The rats are housed at a constant temperature (22°C) on a 12–h light/dark cycle with food and tap water. The animals are arranged into three groups: WKY rats (the control group), DOX rats and DOX rats treated with HSF1A. Each group contain five animals. The DOX group is injected with DOX (5 mg/kg) for 6 consecutive weeks intraperitoneal injection to achieve a cumulative dose of 30 mg/kg, which has been well documented to achieve cardiotoxicity. The small molecular HSF1 activator HSF1A (100 mg/kg/day) is injected intraperitoneally.References:[1]. Neef DW, et al. A direct regulatory interaction between chaperonin TRiC and stress–responsive transcription factor HSF1. Cell Rep. 2014 Nov 6;9(3):955–66.[2]. Neef DW, et al. Modulation of heat shock transcription factor 1 as a therapeutic target for small molecule intervention in neurodegenerative disease. PLoS Biol. 2010 Jan 19;8(1):e1000291.[3]. Huang CY, et al. Doxorubicin attenuates CHIP–guarded HSF1 nuclear translocation and protein stability to trigger IGF–IIR–dependent cardiomyocyte death. Cell Death Dis. 2016 Nov 3;7(11):e2455.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。
双去甲氧基姜黄素对小鼠乳腺癌的抗肿瘤作用及机制
双去甲氧基姜黄素对小鼠乳腺癌的抗肿瘤作用及机制李学瑛;徐阳;王秘【期刊名称】《国际医药卫生导报》【年(卷),期】2022(28)16【摘要】目的本研究旨在研究双去甲氧基姜黄素(bisdesmethoxycurcumin,BDMC)对小鼠乳腺癌的影响及机制。
方法采用小鼠乳腺癌4T1细胞,分为Control组及不同剂量(3、9、27μM)BDMC组,通过CCK8法检测BDMC对小鼠乳腺癌4T1细胞增殖的影响,TUNEL染色检测BDMC对4T1细胞凋亡的影响,Western blot检测BDMC对4T1细胞Bax、Bcl-2及cleaved caspase-3表达的影响;采用4T1乳腺癌荷瘤小鼠模型,分为Control组及不同剂量(10、30 mg/kg)BDMC组,检测BDMC对小鼠肿瘤体积及体质量的影响,Western blot检测BDMC对乳腺癌小鼠肿瘤组织Bax、Bcl-2及cleaved caspase-3表达的影响。
采用单因素方差分析。
结果与Control组相比,9、27μM BDMC均能明显抑制4T1细胞增殖(均P<0.01),促进其凋亡(均P<0.01),同时上调细胞Bax/Bcl-2比值及cleaved caspase-3表达(均P<0.01);10、30 mg/kg BDMC均能明显抑制乳腺癌小鼠肿瘤体积的增长(均P<0.05),同时明显上调肿瘤组织Bax/Bcl-2比值及cleaved caspase-3表达(均P<0.05),但对体质量无明显影响。
结论BDMC对乳腺癌小鼠模型具有明显的抗肿瘤作用,其机制与激活线粒体凋亡通路有关。
【总页数】5页(P2311-2315)【作者】李学瑛;徐阳;王秘【作者单位】滨州职业学院健康学院;上海市医药学校生物技术制药系【正文语种】中文【中图分类】R73【相关文献】1.双去甲氧基姜黄素抑制肝癌细胞增殖并诱导凋亡的机制2.双脱甲氧基姜黄素抗血管生成作用分子学机制研究3.双去甲氧基姜黄素对四氯化碳致小鼠急性肝损伤的保护作用及机制4.双脱甲氧基姜黄素对db/db小鼠胰岛素抵抗和糖稳态作用及机制研究5.双去甲氧基姜黄素对四氯化碳致小鼠急性肝损伤的保护作用及机制因版权原因，仅展示原文概要，查看原文内容请购买。
Gelucire-14-44-SDS-MedChemExpress
Inhibitors, Agonists, Screening LibrariesSafety Data Sheet Revision Date:Nov.-23-2018Print Date:Nov.-23-20181. PRODUCT AND COMPANY IDENTIFICATION1.1 Product identifierProduct name :Gelucire 14/44Catalog No. :HY-Y1892CAS No. :121548-04-71.2 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 mixtureNot a hazardous substance or mixture.2.2 GHS Label elements, including precautionary statementsNot a hazardous substance or mixture.2.3 Other hazardsNone.3. COMPOSITION/INFORMATION ON INGREDIENTS3.1 SubstancesSynonyms:NoneFormula:N/AMolecular Weight:N/ACAS No. :121548-04-74. 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:Pure form-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 White to off-white (Oil)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 2018 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。
黄芩素通过调节HIF-1α
黄芩素通过调节HIF -1α/VEGF 信号通路抑制类风湿关节炎大鼠的炎症反应和病理性血管生成*杜红丽1，张晨宇1，赵清2△［1河南中医药大学第五临床医学院（郑州人民医院）风湿免疫科，河南郑州450053；2河南大学淮河医院风湿免疫科，河南开封475099］［摘要］目的：探讨黄芩素（BA ）调节缺氧诱导因子1α（HIF -1α）/血管内皮生长因子（VEGF ）信号通路对类风湿关节炎（RA ）大鼠炎症反应和病理性血管生成的影响。
方法：按照随机数字表法将SD 大鼠分为对照（control ）组、模型（model ）组、低剂量（10mg/kg ）BA （BA -L ）组、高剂量（30mg/kg ）BA （BA -H ）组、雷公藤多苷片（TWP ；6.25mg/kg ）组和BA -H+HIF -1α激动剂二甲基草酰甘氨酸（DMOG ；40mg/kg ）组，每组12只。
除control 组外，其它组大鼠均采用II 型胶原蛋白-完全弗氏佐剂法诱导RA 大鼠模型。
第2次免疫24h 后开始给药处理，每天给药一次，持续4周。
检测大鼠在给药第0、7、14和28天时的足趾肿胀度，计算关节炎指数；计算大鼠胸腺和脾脏指数；HE 染色检测大鼠踝关节滑膜组织病理损伤；ELISA 法检测大鼠踝关节滑膜组织中肿瘤坏死因子α（TNF -α）和白细胞介素6（IL -6）水平；免疫组化检测大鼠踝关节滑膜组织中VEGF 和VEGF 受体2（又称激酶插入域受体，KDR ）表达；Western blot 检测各组大鼠踝关节滑膜组织中HIF -1α和VEGF 蛋白表达。
结果：与control 组比较，model 组大鼠踝关节滑膜组织病理损伤严重，足趾肿胀度、关节炎指数、胸腺和脾脏指数，以及滑膜组织TNF -α、IL -6、VEGF 、KDR 、HIF -1α和VEGF 水平均显著升高（P <0.05）；与model 组比较，BA -L 组、BA -H 组和TWP 组对应指标变化趋势与上述相反（P <0.05）；BA -H 组与TWP 组比较，上述指标变化差异无统计学意义（P >0.05）；DMOG 减弱了BA -H 对RA 大鼠炎症反应和病理性血管生成的抑制作用。
美国Medchemexpress化合物库(小分子库)_Medchemexpress_(MCE中国)
美国Medchemexpress化合物库（小分子库）-原装进口，现货供
应，提供组合定制服务
品牌：Medchemexpress （MCE）
保存条件：-20℃
供应商：MCE中国
数量：大量
保质期：2年
Size：
Pre-dissolved DMSO/Solid（Or dry solid）
100 uL/well (10 mM solution)
200 uL/well (10 mM solution)
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硫辛酸注射液联合胰激肽原酶肠溶片对DPN_的临床疗效及生存质量的影响
DOI：10.16658/ki.1672-4062.2024.01.174硫辛酸注射液联合胰激肽原酶肠溶片对DPN的临床疗效及生存质量的影响王莉，朱海峰濉溪县中医医院内分泌科，安徽淮北235100[摘要]目的探讨硫辛酸注射液联合胰激肽原酶肠溶片对2型糖尿病周围神经病变（Diabetic Peripheral Neu⁃ropathy， DPN）患者的临床疗效、生存质量及安全性的影响。
方法选取2021年2月—2022年4月濉溪县中医医院60名DPN患者作为研究对象。
通过随机数表法分为两组，每组30例。
对照组采用常规治疗，观察组在对照组基础上加用硫辛酸注射液和胰激肽原酶肠溶片治疗。
比较两组患者的神经病变评分、神经电生理指标、生存质量评分、安全性指标和不良反应发生率。
结果治疗后，观察组神经病变评分（6.2±0.9）分低于对照组（7.6±1.1）分，差异有统计学意义（t=5.438，P<0.05）；观察组神经电生理指标、生存质量评分、安全性指标均优于对照组，差异有统计学意义（P均<0.05）；两组患者不良反应发生率比较，差异无统计学意义（P>0.05）。
结论硫辛酸注射液联合胰激肽原酶肠溶片对DPN患者有良好的临床疗效，能够改善神经功能、改善神经电生理指标、提高生存质量，且安全性高。
[关键词] 硫辛酸注射液；胰激肽原酶肠溶片；2型糖尿病周围神经病变；临床疗效[中图分类号] R587.2 [文献标识码] A [文章编号] 1672-4062（2024）01（a）-0174-05Effect of Lipoic Acid Injection Combined with Pancreatic Kininogenase Enteric-coated Tablets on Clinical Efficacy and Quality of Survival in DPN WANG Li, ZHU HaifengDepartment of Endocrinology, Suixi County Hospital of Traditional Chinese Medicine, Huaibei, Anhui Province, 235100 China[Abstract] Objective To investigate the effects of lipoic acid injection combined with pancreatic kininogenase enteric-coated tablets on the clinical efficacy, quality of survival and safety of patients with type 2 diabetic peripheral neuropathy (DPN). Methods 60 DPN patients admitted to Suixi County Hospital of Traditional Chinese Medicine from February 2021 to April 2022 were selected as the study objects. They were divided into two groups with 30 cases in each group by random number table method. The control group received conventional treatment, and the observation group was treated with lipoic acid injection and pancreatic kininogenase enteric-coated tablets on the basis of control group. Neuropathy score, neuroelectrophysiological index, quality of life score, safety index and incidence of adverse reactions were compared between the two groups. Results After treatment, the neuropathy score of observation group (6.2±0.9) points was lower than that of control group (7.6±1.1) points, and the difference was statistically significant (t= 5.438, P<0.05). Neuroelectrophysiological indexes, quality of survival scores and safety indexes of the observation group were better than those of the control group, and the differences were statistically significant (all P<0.05). There was no significant difference in the incidence of adverse reactions between the two groups (P>0.05). Conclusion Li⁃[作者简介]王莉（1982-），女，本科，主治医生，研究方向为糖尿病周围神经病变。
Expression, Purification and Crystallization of
Expression, Purification and Crystallization of the Mycobacterium Tuberculosis HSP16.3 Molecular Chaperone Background of Mycobacterium Tuberculosis HSP16.3HSP16.3, a 16.3 kDa protein from Mycobacterium Tuberculosis, was originally identified as a prominent antigen (Kingston et al., 1987). During the stationary phase, HSP16.3 is maximally expressed and becomes a main protein of the latent phase (Yuan et al., 1996). Previous studies showed that HSP16.3 can make the cell structure stable and prevent stationary Mycobacterium Tuberculosis from autolysing (Cunningham et al., 1998). In previous studies, HSP16.3 was found as one of theα-crystallin-related small heat shock proteins (sHSP) with molecular chaperone activity. Experiments in vitro revealed that HSP16.3 can suppress the thermal aggregation of citrate synthase at 39.5˚C, without consumption of A TP (Chang et al., 1996).Now the Mycobacterium Tuberculosis HSP16.3 gene was cloned to the plasmid pSTE-HSP16.3, and transformed to E.Coli. BL21(DE3) strain.Material and MethodExpressionThings to have ready before Starting.-Plate or glycerol culture-Sterile LB 25ml in a 50mL shaker flasker, 250ml in a 500mL shaker flasker, all together autoclaved, antibiotic added afterword.- antibiotic and sterile water- TipsPrepare the LB and autoclave:Fomula of the LB medium for 1 Liter:Bacto Tryptone (BT) 10 gBacto Y east Extract (BYE) 10 gNaCl 10gThe LB medium, dd H2O and the tips all together autoclaved at 121 ˚C for 20 minutes.Method:1 Innoculate 25 ml LB Medium ( containing 100 ug) and grow culture overnight(37˚C, 200rpm).2 Next morning inoculate 250 ml prewarmed LB Medium ( containing 100 ug) with the 25 ml overnight culture and grow at 37 ˚C, 200rpm, HSP16.3 was overexpressed in soluble form intracellularly without IPTG induction.3 Incubate the Culture for 10 hours before havesting the cell at 4000 g for 20 minutes.4 Resuspend the cell pellet in 30 ml Butter A and freeze the Sample in -80˚C refigerator.PurificationDE52 Ion-Exchange columnThings to have ready before Starting.-Butter A: 50 mM Imidazole pH 6.5 (1 liter)-Butter B: 50 mM Imidazole pH 6.5 , 300mM NaClall together Fitrate with 0.2 um membrane.- DE52 medium , column ,Gradient maker, UV-monitor and Fractioner- TipsMethod:1 Thaw the cell pellet and vortex .2 Add 0.4ml 100 mM PMSF and sonicate (400kw, 4s-6s 50 cycle* 5 )3 Centrifuge 15000 rpm, 30 minutes to pellet debris4 Transfer supernatant to a 50 ml conicale tube and discard the pellet.5 The supernatant dilute to 50 ml with Buffer A and then load to DE52 ion-exchange columns (20ml), which was pre-equibrated with 100ml Buffer A. And then wash the unbound proteins with 100 ml Buffer A.6 Elute the protein with a linear gradient : 200ml buffer A plus 200ml buffer B, 2ml/min, 6ml each fraction.7 Run 15% SDS-PAGE to determine the HSP16.3 peak.Desalting by dialysis1 Preparation of the dialysis tubeCut the tube in a suitable length (20-30 cm)Boil the tube in solution containing 10 mM NaHCO3 for a few minutes.Boil the tube in solution containing 10 mM EDTA for a few minutes.Rasin the tube with de-ion water2 Pool the HSP16.3 peak and dialysis the Sample against 1000ml Buffer A for more than 6hours.Q-Separose (HP) Ion-Exchange Column1 load the sample to Q-Separose (HP) Ion-Exchange column (20ml), which was pre-equibrated with 100ml Buffer A. And then wash the unbound proteins with 100 ml Buffer A.2 Elute the protein with a linear gradient : 200ml buffer A plus 200ml buffer B, 2ml/min, 6ml each fraction.3 Run 15% SDS-PAGE to determine the purity of the HSP16.3 peak.Gel filtration ColumnThe HSP peak was a final volumn 0.3ml and then run though a Superdex75 (HR, 10/30mm) gel filtration column in 150mM NaCl and 5mM Imdazole, pH6.5. Crystallization1 The purified HSP16.3 was solvent-exchanged to water and concentrated to 20mg/ml before crystallization trails (Bradford). All the crystallization trials were carried out using the hanging-drop vapor-diffusion method at 291K: drops consisted of2 microlitres of HSP16.3 protein solution plus 2 microlitres of the precipitant. The drops were equilibrated against 0.2 ml precipitant at room temperature. The crystallization conditions were investigated with a PEG4000 Kit.Result and discussionThe purity of the final HSP16.3 was over 95% by SDS-PAGE. The crystallization trials of HSP16.3 yielded Cubic crystals with a size of 0.8*0.8*0.6mm in a few days.20040060080010001200mAUBuffer Tris-HCL pH 8.5 Precipitant PEG 4000 MethodV apor Diffusion Temperature 293 K Size0.8*0.8*0.6mmReferencesChang Z., Primm, T.P., Jakana J., Lee H. I., Serysheva I., Chiu W., Gilber H. F., Quiocho F. A., (1996) J Biol Chem 271:7218-7223Cunningham A. F., Spreadbury C. L., (1998) J. Bacteriol. 184:801-808Kingston A. E., Salgame P. R., Mitchison N.A., Colston M. J. (1987) Infect. Immun 55,3149-3154Yuan Y., Crane D. D., Barry C. E. III (1996) J Bacteriol178: 4484-4492。
德谷门冬双胰岛素注射液治疗2_型糖尿病临床效果及安全性探讨
DOI：10.16658/ki.1672-4062.2023.17.098德谷门冬双胰岛素注射液治疗2型糖尿病临床效果及安全性探讨林生，谢平，陈予福州市长乐区人民医院内分泌科，福建福州350200[摘要]目的研究德谷门冬双胰岛素注射液治疗2型糖尿病的临床效果及安全性。
方法选取于2022年7月—2023年4月福州市长乐区人民医院收治的2型糖尿病患者98例为研究对象，采用随机抓阄法分为两组，每组49例。
两组均联用常规降糖药物治疗，对照组采用甘精胰岛素注射液治疗，观察组采用德谷门冬双胰岛素注射液治疗。
对比两组临床治疗效果、临床症状好转时间和胰岛素用量情况、糖代谢指标、胰岛素功能指标、不良反应发生情况、心血管不良事件发生情况。
结果观察组总有效率高于对照组，差异有统计学意义（P<0.05）。
观察组尿酮体转阴时间、血糖达标时间、胰岛素用量均优于对照组，差异有统计学意义（P< 0.05）。
观察组空腹血糖、餐后2 h血糖、糖化血红蛋白均低于对照组，差异有统计学意义（P<0.05）。
观察组胰岛β细胞功能指数高于对照组，胰岛素抵抗指数、空腹胰岛素低于对照组，差异有统计学意义（P<0.05）。
两组恶心呕吐、倦怠乏力、低血糖总发生率比较，差异无统计学意义（P>0.05）。
两组心绞痛、心力衰竭总发生率比较，差异无统计学意义（P>0.05）。
结论德谷门冬双胰岛素注射液治疗2型糖尿病临床效果显著优于甘精胰岛素注射液，但是治疗安全性无显著变化。
[关键词] 2型糖尿病；德谷门冬双胰岛素注射液；不良反应；心血管不良事件[中图分类号] R59 [文献标识码] A [文章编号] 1672-4062（2023）09（a）-0098-04Discussion on the Clinical Effect and Safety of Insulin Degludec and Insu⁃lin Aspart Injection in the Treatment of Type 2 Diabetes MellitusLIN Sheng, XIE Ping, CHEN YuDepartment of Endocrinology, Changle District People's Hospital, Fuzhou, Fujian Province, 350200 China[Abstract] Objective To study the clinical effect and safety of insulin degludec and insulin aspart injection in the treatment of type 2 diabetes mellitus. Methods A total of 98 patients with type 2 diabetes admitted to Fuzhou Changle District People's Hospital from July 2022 to April 2023 were selected as the study objects and divided into two groups with 49 cases in each group by random lottery method. Both groups were treated with conventional hypoglycemic drugs, the control group was treated with insulin glargine injection, and the observation group was treated with Degu asparton double insulin injection. The clinical therapeutic effect, time of improvement of clinical symptoms, insulin dosage, glucose metabolism index, insulin function index, occurrence of adverse reactions and cardiovascular adverse events were compared between the two groups. Results The total effective rate of the observation group was higher than that of the control group, and the difference was statistically significant (P<0.05). The time of urine ketone body turning negative, blood glucose reaching standard and insulin dosage in observation group were better than those in control group, and the differences were statistically significant (P<0.05). Fasting plasma glucose, 2-hour postprandial blood glucose and glycated hemoglobin in the observation group were lower than those in the control group, and the differences were statistically significant (P<0.05). The function index of islet β cells in observation group was higher than that in control group, the insulin resistance index and fasting insulin was lower than that in control group, the dif⁃ference was statistically significant (P<0.05). There was no statistically significant difference in the total incidence of [作者简介]林生（1981-），男，本科，副主任医师，研究方向为糖尿病及其并发症的相关临床研究。
SKI-II-LCMS-20601-MedChemExpress
=====================================================================Acq. Operator : Su Xiao Ying(LCMS-02) Seq. Line : 46Acq. Instrument : HY-LCMS-02 Location : P1-F-04Injection Date : 6/2/2016 1:42:02 PM Inj : 1Inj Volume : 3.000 µlAcq. Method : D:\AGLIENT 1260\DATA\20160602\20160602 2016-06-02 08-59-29\100-1000MS+3MIN- 1.5_(0.02%FA).MLast changed : 6/2/2016 8:59:29 AM by Su Xiao Ying(LCMS-02)Analysis Method : D:\AGLIENT 1260\DATA\20160602\20160602 2016-06-02 08-59-29\100-1000MS+3MIN- 1.5_(0.02%FA).M (Sequence Method)Last changed : 6/3/2016 10:10:48 AM by Su Xiao Ying(LCMS-02) (modified after loading)M ethod Info : HY-365_5HO1RS,M,A-RP-108，210nm,23minCatalog No : HY-13822 Batch#20601 A-RP-153Additional Info : Peak(s) manually integratedmin*0.511.522.53mAU 020040060080010001200*DAD1 B, Sig=214,4 Ref=off (D:\AGLIENT 1260\DATA\20160602\20160602 2016-06-02 08-59-29\BIZ2016-602-WJ2.D)2.2222.4112.526===================================================================== Area Percent Report =====================================================================Sorted By : Signal Multiplier : 1.0000Dilution : 1.0000Do not use Multiplier & Dilution Factor with ISTDsSignal 1: DAD1 B, Sig=214,4 Ref=offSignal has been modified after loading from rawdata file!Peak RetTime Type Width Area Height Area # [min] [min] [mAU*s] [mAU] %----|-------|----|-------|----------|----------|--------| 1 2.222 MM 0.0425 3502.45972 1374.85510 98.6938 2 2.411 MM 0.0778 29.06973 6.23061 0.8191 3 2.526 MM 0.0558 17.28664 5.16699 0.4871Totals : 3548.81609 1386.25269===================================================================== *** End of Report ***=====================================================================Acq. Operator : Su Xiao Ying(LCMS-02) Seq. Line : 46Acq. Instrument : HY-LCMS-02 Location : P1-F-04Injection Date : 6/2/2016 1:42:02 PM Inj : 1Inj Volume : 3.000 µlAcq. Method : D:\AGLIENT 1260\DATA\20160602\20160602 2016-06-02 08-59-29\100-1000MS+3MIN- 1.5_(0.02%FA).MLast changed : 6/2/2016 8:59:29 AM by Su Xiao Ying(LCMS-02)Analysis Method : D:\AGLIENT 1260\DATA\20160602\20160602 2016-06-02 08-59-29\100-1000MS+3MIN- 1.5_(0.02%FA).M (Sequence Method)Last changed : 6/2/2016 2:36:16 PM by Su Xiao Ying(LCMS-02) (modified after loading)M ethod Info : HY-365_5HO1RS,M,A-RP-108，210nm,23minCatalog No : HY-13822 Batch#20601 A-RP-153Additional Info : Peak(s) manually integratedmin0.511.522.5350000100000150000200000250000300000 MSD1 TIC, MS File (D:\AGLIENT 1260\DATA\20160602\20160602 2016-06-02 08-59-29\BIZ2016-602-WJ2.D) ES-API, Pos, Scan2.218MS Signal: MSD1 TIC, MS File, ES-API, Pos, Scan, Frag: 50 Spectra averaged over upper half of peaks. Noise Cutoff: 1000 counts.Reportable Ion Abundance: > 10%.Retention Mol. Weight Time (MS) MS Area or Ion2.218 1761020 305.00 I 304.10 I 303.10 Im/z10020030040050060070020406080100*MSD1 SPC, time=2.198:2.271 of D:\AGLIENT 1260\DATA\20160602\20160602 2016-06-02 08-59-29\BIZ2016-602-WJ2.D ES-API, Max: 157077306.0305.0 303.1*** End of Report ***。
聚二甲基硅氧烷基质微流控芯片封接技术的研究
V o l.23高等学校化学学报 N o.12 2002年12月 CH E M I CAL JOU RNAL O F CH I N ESE UN I V ER S IT IES 2243～2246 聚二甲基硅氧烷基质微流控芯片封接技术的研究叶美英,方 群,殷学锋,方肇伦(浙江大学化学系,微分析系统研究所,杭州310028)摘要 考察了聚二甲基硅氧烷(Po lydi m ethylsiloxane,PDM S)预聚体与固化剂间的配比、固化温度及固化时间对PDM S芯片封接强度的影响,得出PDM S芯片封接的最佳条件基片和盖片所用PDM S预聚体与固化剂质量配比分别为10∶1与5∶1,固化温度为75℃,固化时间分别为35～50m in和25～40m in,封接后继续加热60m in.在该条件下封接制作的微芯片历经半年50多次的分析、冲洗及抽液后未见明显损坏,足以满足一般分析任务的要求,并将芯片成功用于两种氨基酸的快速毛细管电泳分离.关键词 聚二甲基硅氧烷(PDM S);微流控芯片;芯片封接中图分类号 O657 文献标识码 A 文章编号 025120790(2002)1222243204微流控芯片分析(M icroflu idic ch i p analysis)是微全分析系统[1,2](M icro to tal analysis system)或称芯片实验室(L ab2on2a2ch i p)的重要组成部分,已引起了人们的普遍关注和兴趣.玻璃具有优良的光学和电渗等性能,已被广泛应用于制作微流控芯片[1,2].但制作玻璃微流控芯片的光刻和蚀刻技术工艺冗长、费时,需要超净环境,芯片键合难度大,材料易碎且成本较高,因此,高分子聚合物已成为制作微流控芯片的重要材料[3].由于聚二甲基硅氧烷(Po lydi m ethylsiloxane,PDM S)能透过300nm以上的紫外和可见光,并具有无毒、用浇注法能复制微通道、加工简便快速和芯片成本低等特点,是目前微流控分析芯片制备中使用较多的高聚物材料[3～7].PDM S芯片通常采用自然封接方法[6]或表面处理后进行封接[4].前者是利用两片PDM S之间的自然亲和性,无需粘接剂,只是简单地将复制了微通道的PDM S基片和PDM S盖片贴合即可完成芯片的封合[6].这种方法虽然简单,但封接强度不高,通常小于10g c m.在实际使用中易因加液、抽液及清洗等操作造成两片PDM S相互脱离.后者通常采用氧等离子体照射两片PDM S的表面后立即封接,虽然可达到两片PDM S的永久粘接,但需要较特殊的设备[4].U nger等[5]用PDM S制作了微阀及微泵,通过使用不同的PDM S与固化剂的配比获得了较高的粘接强度,但未对影响粘接强度的因素进行系统的研究.本文系统地考察了不同PDM S预聚体和固化剂的质量配比、温度及时间对PDM S的粘接性质的影响,优化了Sylgard184型PDM S的最佳封接条件.用简便的方法制成了具有较高粘接强度的PDM S微流控芯片,并成功地用于混合氨基酸的毛细管电泳分离.1 实验部分1.1 仪器与试剂“十”字通道型(通道宽75Λm,高15Λm;分离通道长30mm,进样通道长10mm)单晶硅阳模(东北大学分析科学研究中心);XTB21型体视镜(南京江南光电股份有限公司);KGB22型可调式恒温电热板(沈阳森华理化仪器研究所);真空泵(浙江黄岩医疗器械厂);367型A r离子激光器(488nm,南京电子管厂);自制微芯片用激光诱导荧光检测系统及多触点高压电源[8].Sylgard184型PDM S预聚体及固化剂(Dow Co rn ing Co rp.,U SA);异硫氰酸酯荧光素(F ITC, A cro s O rgan ics,N J,U SA);精氨酸(A rg)及苯丙氨酸(Phe)(上海康达氨基酸厂).收稿日期:2002201215.基金项目:国家自然科学基金(批准号:20299030)资助.联系人简介:殷学锋(1945年出生),男,硕士,教授,博士生导师,主要从事微流控分析研究.E2m ail:cheyinxf@m 1.2 实验操作1.2.1 芯片粘接强度测定试验 将两片洁净的载玻片置于恒温电热板上,四周围以铝合金薄片制的围框,以防止液体PDM S 外流.将不同质量比的PDM S 预聚体与固化剂混合均匀,室温下在真空干燥箱中脱气10m in ,然后分别浇注于载玻片上,形成厚度约0.7mm 的液层.在选定温度范围(25～125℃)下加热固化.达到预定的固化时间后,各取宽1c m 的PDM S 片,将两者的下表面对粘后置于电热板上再加热约1h .冷却后用T 型剥离法[9]测定两片PDM S 间的粘接强度.1.2.2 PDM S 微芯片的制作 将平板玻璃片与带有凸出的“十”字形微通道的单晶硅阳模置于恒温电热板上,四周围以铝合金薄片制成的围框.同上述方法,将PDM S 预聚体 固化剂配比(质量比,下同)分别为5∶1与10∶1的液体混合物脱气10m in 后,分别浇注于平板玻璃片与单晶硅阳模上形成1mm 厚液层,在75℃下加热固化,达到预定的固化时间后,分别从平板玻璃片和硅阳模上取下盖片和带微通道的PDM S 基片,用打孔器在基片上通道的末端打4个直径为4mm 的储液孔.将两片对粘,再加热1h 至两者牢固地粘合,即完成芯片的制作.具体的制作流程见图1.F ig .1 Sche matic of m icrofabr ication of PDM S m icrof luidic ch ip1.2.3 PDM S 微流控芯片用于氨基酸的分离 以PDM S 微流控芯片、多触点高压电源及激光诱导荧F ig .2 Block di agram of PDM S m icroch ip analysis syste m 光检测器构成芯片毛细管电泳分离2激光诱导荧光检测氨基酸分析系统,其实验装置见图2.系统工作时,在芯片上储液池1,2和4内加入5mm o l L 硼砂缓冲液(pH =9.3),向储液池3内加入F ITC 以标记氨基酸混合溶液.将高压电源的4个电极分别插入储液池内.进样时,在液池2与3之间施加136V 电压,进样时间10s ;分离时,在储液孔1与4之间施加250V 电压,有效分离距离2.5c m .荧光检测系统激发波长488nm ,发射波长520nm .其它具体操作方法参见文献[8].2 结果与讨论2.1 固化温度和配比对固化速度的影响考察了PDM S 预聚体 固化剂质量配比为50∶1,25∶1,10∶1,5∶1及2.5∶1在固化温度为25,50,75,100及120℃下的固化速度.Sylgard 184型PDM S 推荐的配比为10∶1,固化温度50～100℃.实验结果表明,高配比(如50∶1和25∶1)的PDM S 在25～120℃范围内加热超过24h 仍未固化,表现为胶体较软,脱模时与单晶硅阳模有粘连,不能形成完整的微通道.配比在10∶1以下的PDM S 固化速度与固化温度关系示于图3.在100℃时,配比为10∶1以下的PDM S ,在10m in 内可基本固化;在75℃时,30m in 内基本固化;即使在50℃时,5h 内也已基本固化.但在常温时(25℃),通常需要数十小时才可达到PDM S 的基本固化.不同配比的PDM S ,在同一温度下,固化速度也有差异,75℃时,10∶1,5∶1及2.5∶1配比的PDM S 基本固化时间分别为25,20和10m in .由此可知,在一定固化温度下,PDM S 预聚体固化剂4422 高等学校化学学报V o l.23F ig .3 The effects of cur i ng te m perature and mass ratioof PDM S to cur i ng agen t on cur i ng ti m e 配比愈高,PDM S 固化速度愈慢;当PDM S 预聚体 固化剂配比保持不变时,固化温度愈高,PDM S固化速度愈快.过高的PDM S 预聚体 固化剂配比(如50∶1和25∶1)及过低的固化温度均会造成PDM S 固化速度过慢而难以固化和脱模,而过低的配比和过高的固化温度易造成固化速度过快,不易控制实验条件.因此,在以下的实验中,使用10∶1与5∶1两种PDM S 预聚体 固化剂配比及75℃固化温度,来进一步考察固化时间对PDM S 芯片粘接强度的影响.2.2 PDM S 芯片的封接本实验考察了不同固化时间(25～150m in )对不同PDM S 预聚体 固化剂配比封接强度的影响.结果如表1所示,其中PDM S 基片与盖片的配比分别为10∶1和5∶1,t 1为基片的固化时间,t 2为盖片的固化时间,固化温度75℃.F ig .4 Electrophoresis separation of F I TC labeled am i no ac ids on the PDM S m icrof luidic ch ipBuffer :5mmo l L sodium bo rate ,pH =9.2;effective length ofseparati on channel :2.5c m ;separating field strength :80V c m .Samp le concentrati on (mmo l ・L -1):A rg 10,Phe 10,F ITC 20.由表1可见,当t 1=35～50m in ,t 2=25～40m in 时,PDM S 芯片的粘接强度最高,长于上述时间,粘接强度均有不同程度地下降.尤其当固化时间较长时,下降更为明显.表明PDM S 需要在固化不完全的情况下才能较好地粘接.这与粘接的扩散理论[10]相符合,即由于基片和盖片中PDM S 与固化剂的配比不同,因此在它们的界面处产生分子扩散,长链分子或其个别链段由于浓度梯度相互扩散到对方的内部,使粘附界面消失,形成一个强有力的结合交织网络过渡区.随着固化时间增长,PDM S 的硅氧键不断加长并进一步交联,使链段分子的运动减小,从而扩散困难,因此粘力减小.但在固化过于不完全的情况下,PDM S 仍有部分液体的性质,无法完整地从阳模或平板玻璃片上揭下,且粘接时易使通道变形,因此固化时间也不宜过短.Table 1 The effect of cur i ng ti m e on adhesive strengthA dhesive strength(g ・c m -1)Curing ti m e 3t 1 m in t 2 m in A dhesive strength (g ・c m -1)Curing ti m e 3t 1 m in t 2 m in 25—30352510—15958525—30504010—1512511515—2065555—10150135 3Curing temperature :75℃;t 1:the curing ti m e of upper PDM S w afer (10∶1rati o )befo re adhesi on ;t 2:the curing ti m e of low er PDM S w afer (5∶1rati o )befo re adhesi on . 实验中还观察到,两片PDM S 封接后需要继续加热一段时间以增加粘接强度,一般控制在60m in ,继续延长加热时间,粘接强度不会有明显改变.本实验还考察了在同样条件下相同配比PDM S芯片的粘接强度.由于在界面处PDM S 与固化剂的配比相同,相互扩散的趋势较小,这样制得的芯片最高粘接强度通常在10～15g c m 之间.比本实验最高粘接强度25～30g c m 小2～3倍.2.3 PDM S 芯片的实际应用将上述优化条件下制作的“十”字通道PDM S 微芯片应用于F ITC 标记的精氨酸(A rg )和苯丙氨酸(Phe )混合物的芯片毛细管电泳分离,结果见图4.芯片经过半年的使用,即500余次的进样和分离操作以及50多次的冲洗、抽液后,仍未有明显的损5422N o .12叶美英等:聚二甲基硅氧烷基质微流控芯片封接技术的研究 6422 高等学校化学学报V o l.23坏和脱离.芯片封接强度完全可以满足一般分析任务的要求.参 考 文 献[1] M anz A.,H arrison D.J.,V erpoo rte E.M.J.et a l..Ch rom atogr.[J],1992,593:253—258[2] H arrison D.J.,M anz A.,Fan Z.et a l..A nal.Chem.[J],1992,64:1926—1932[3] Soper S.A.,Fo rd S.M.,Q i S.et a l..A nal.Chem.[J],2000,72:643—651[4] D uffy D.C.,M c Donald J.C.,Schueller O.J.A.et a l..A nal.Chem.[J],1998,70:4974—4984[5] U nger M.A.,Chou H.,T ho rsen T.et a l..Science[J],2000,288:113—116[6] J I N Peng(金 鹏),TAN J iu2B in(谭久彬),L I U Yan(刘 岩).M icrom echanical T echno logy(微细加工技术)[J],2001,3:31—34[7] XU Yi(徐 溢),E ijkel J.C.T.,M anz A..Chem.J.Ch inese U niversities(高等学校化学学报)[J],2000,21(7):1028—1034[8] Fang Q.,Xu G.M.,Fang Z.L..A nal.Chem.[J],2002,74:1223—1231[9] YAN G Yu2Kun(杨玉 ),L I AO Zeng2Kun(廖增琨),YU Yun2Zhao(余云照)et a l..Synthesized A dhesives(合成胶粘剂)[M],Beijing:Science P ress,1980:149—572[10] CH EN D ao2Yi(陈道义),ZHAN G Jun2Ying(张军营).T he Fundam ental P rinci p le of A dhesi on(胶接基本原理)[M],Beijing:Sci2ence P ress,1992:1—253Stud ies on Bond i ng Techn iques for Poly(d i m ethylsiloxane)M icrof lu id ic Ch ipsYE M ei2Y ing,FAN G Q un,Y I N Xue2Feng3,FAN G Zhao2L un (Institu te of M icroanaly sis S y ste m,D ep art m ent of Che m istry,Z hej iang U niversity,H ang z hou310028,Ch ina)Abstract In th is p ap er the p rocedu re w as discribed fo r enclo sing PDM S sub strate con tain ing m i2 cro structu res w ith a flat p iece of PDM S cover p late to fab ricate PDM S m icroflu idic ch i p s.T he effects of p ropo rti on s of PDM S p repo lym er and cu ring agen t,cu ring tem peratu re and ti m e on the bonding strength of PDM S w afers w ere investigated.T he op ti m al m ass p ropo rti on s w ere10∶1fo r sub strate and5∶1fo r cover p late.T he op ti m al cu ring ti m e fo r sub strate and cover p late w as35—50m in and 25—40m in,resp ectively,at75℃.T he su rface of the sub strate and that of the cover p late seal tigh t2 ly and irreversib ly w hen b rough t in to clo se con tact and con tinue cu red fo r60m in at75℃.T he ch i p s have been u sed successfu lly fo r the separati on of tw o F ITC labeled am ino acids and w o rked w ell w ith2 in a p eri od of six m on th s w ith m o re than50cycles of operati on s invo lving so lu ti on loading in the chan2 nel and channel w ash ing.Keywords Po ly(di m ethylsiloxane)(PDM S);M icroflu idic ch i p;Ch i p sealing(Ed.:A,G)。
德谷门冬双胰岛素注射液治疗2_型糖尿病的疗效及安全性研究
DOI：10.16658/ki.1672-4062.2023.19.084德谷门冬双胰岛素注射液治疗2型糖尿病的疗效及安全性研究戴卉，张开凤，朱凤丽江苏省镇江市丹徒区人民医院内分泌科，江苏镇江212000[摘要]目的探讨德谷门冬双胰岛素注射液在2型糖尿病中的效果以及安全性。
方法选取2022年1月—2023年7月江苏省镇江市丹徒区人民医院收治的62例2型糖尿病患者为研究对象，按随机数表法分为对照组（n=31）和观察组（n=31）。
对照组患者接受门冬胰岛素30注射液治疗，观察组患者接受德谷门冬双胰岛素注射治疗。
对比两组患者临床疗效、血糖变化和不良反应发生率。
结果观察组治疗有效为96.77%，高于对照组的77.42%，差异有统计学意义（χ2=5.167，P=0.023）。
治疗前，两组患者血糖水平比较，差异无统计学意义（P>0.05）；治疗后，两组患者血糖水平均改善，且观察组血糖指标低于对照组，差异有统计学意义（P< 0.05）。
观察组不良反应发生率低与对照组，差异有统计学意义（P<0.05）。
结论德谷门冬双胰岛素的应用可以明显改善2型糖尿病患者血糖水平，疗效更为确切，且安全性更高，不会增加用药后不良反应。
[关键词] 2型糖尿病；德谷门冬双胰岛素；门冬胰岛素30注射液；安全性[中图分类号] R587 [文献标识码] A [文章编号] 1672-4062（2023）10（a）-0084-04Study on the Efficacy and Safety of Insulin Degludec and Insulin Aspart Injection in the Treatment of Type 2 Diabetes MellitusDAI Hui, ZHANG Kaifeng, ZHU FengliDepartment of Endocrinology, Zhenjiang Dantu District People's Hospital, Zhenjiang, Jiangsu Province, 212000 China [Abstract] Objective To explore the effect and safety of insulin degludec and insulin aspart injection in type 2 diabe⁃tes mellitus.Methods 62 patients of type 2 diabetes mellitus patients admitted to Zhenjiang Dantu District People's Hospital, Jiangsu Province from January 2022 to July 2023 were selected as study objects and divided into the control group (n=31) and the observation group (n=31) by taking the random number table method. The patients in the control group were treated with insulin aspart 30 injection and the patients in the observation group were treated with insulin degludec and insulin aspart injection. Compared the clinical efficacy, the changes in blood glucose and the incidence of adverse reactions between the two groups of patients.Results The treatment effectiveness of the observation group was 96.77%, which was higher than that of the control group, which was 77.42%, and the difference was statistically significant (χ2=5.167, P=0.023). There was no statistically significant difference in blood glucose levels between the two groups before treatment (P>0.05). After treatment, blood glucose levels improved in both groups, and the level of blood glucose in the observation group were lower than those in the control group, and the difference was statistically significant (P<0.05). The incidence of adverse reactions in the observation group was lower than that in the control group, and the difference was statistically significant (P<0.05).Conclusion The application of insulin degludec and in⁃sulin aspart can significantly improve the blood glucose level of patients with type 2 diabetes mellitus, the efficacy is more accurate, and the safety is higher, and it will not increase the occurrence of adverse reactions after the use of medication.[作者简介]戴卉（1985-），女，本科，主治医师，研究方向为内分泌科。
西格列汀对2型糖尿病患者血清chemerin 水平的影响
西格列汀对2型糖尿病患者血清chemerin 水平的影响马菁菁;罗跃娥;张捷;高雪【期刊名称】《中国实验诊断学》【年(卷),期】2014(000)008【总页数】3页(P1297-1299)【作者】马菁菁;罗跃娥;张捷;高雪【作者单位】天津医学高等专科学校，天津 300222;天津医学高等专科学校，天津 300222;天津医科大学代谢病医院;天津市医药采购中心【正文语种】中文Chemerin是一种新发现的脂肪细胞因子，能够调节脂肪细胞分化，在糖脂代谢中发挥重要作用[1]。
研究发现，血清chemerin与肥胖、代谢综合征、糖尿病的发生密切相关[2]。
西格列汀属于二肽基肽酶-4(DPP-4)抑制剂，通过选择性抑制DPP-4，减少胰高糖素样肽-1(GLP-1)的降解，延长GLP-1的作用时间，促进胰岛素分泌，降低血糖，改善胰岛功能[3]。
本研究旨在观察西格列汀对2型糖尿病(T2DM)患者血清chemerin水平的影响，探讨其在T2DM治疗中的作用机制。
1 对象与方法1.1 对象随机选取2010年-2012年在我院内分泌科门诊就诊的128例T2DM患者，其中男性72例，女性56例，年龄48-65岁。
随机分为常规治疗组和西格列汀组，每组64例。
其中常规治疗组男性38例，女性26例；西格列汀组男性34例，女性30例。
两组在性别、年龄、体质指数(BMI)等方面相比无明显差异。
1.2 方法所有受试患者均采取饮食控制和运动锻炼，对照组服用磺脲类、双胍类或应用胰岛素等降糖药物干预，而干预组则加服西格列汀100 mg/d，干预12周。
观察期间根据血糖水平调整降糖药物，每2-4周门诊随诊1次，将观察期间因转诊等原因无法随访或不按要求服药导致资料不全者剔除。
如无特殊原因，不改变原来的降糖干预方案。
对于合并高血压、高脂血症的患者给予相应的降压、降脂干预。
所有受试者在干预前后均详细测量身高、体重、血压。
留取空腹静脉血，检测空腹血糖(FPG)、餐后2 h血糖(P2hPG)、糖化血红蛋白(HbAlc)、胰岛素(FINS)、血脂；并留取1 ml 血清置于-20℃ 冰箱保存，利用酶联免疫吸附法测定血清chemerin水平，试剂盒均购于美国凤凰公司。
人血浆中非诺贝酸的的HPLC测定及药物动力学研究
人血浆中非诺贝酸的的HPLC测定及药物动力学研究
高志伟;李中东;焦正;施孝金;钟明康
【期刊名称】《中国医药工业杂志》
【年(卷),期】2006(37)1
【摘要】建立了HPLC法测定人血浆中非诺贝酸。
以苄普地尔为内标,采用C18柱,流动相为甲醇-水-10%磷酸(70∶30∶1),检测波长286nm。
非诺贝酸在0.1～
25μg/ml浓度范围内线性关系良好,方法回收率96.8%～105.0%。
24名男性志愿者单剂量口服非诺贝特200mg的药物动力学参数Tmax、Cmax、t1/2和
AUC0→∞分别为(6.02±2.56)h、(5.33±3.81)μg/ml、(23.61±5.98)h和(169.75±126.96)μg·h·ml-1。
【总页数】3页(P32-34)
【关键词】非诺贝特;非诺贝酸;高效液相色谱;测定;药物动力学
【作者】高志伟;李中东;焦正;施孝金;钟明康
【作者单位】复旦大学附属华山医院临床药学研究室
【正文语种】中文
【中图分类】R969.1;O657.72
【相关文献】
1.HPLC-MS/MS测定比格犬血浆中非诺贝酸浓度及其药代动力学研究 [J], 马飞;邢春宇;吴卓娜;孟志云;甘慧;朱晓霞;顾若兰;窦桂芳;王德才
2.HPLC法测定血浆中非诺贝特活性代谢物非诺贝酸的浓度 [J], 徐帆;冯恩富;余昉
3.反相高效液相色谱法测定人血浆中非诺贝特活性代谢物非诺贝酸 [J], 耿立坚;李性天;周密妹;吴国明
4.人血浆中阿比朵尔的HPLC法测定及其药物动力学研究 [J], 杨汉煜;张淑慧;冯小龙
因版权原因，仅展示原文概要，查看原文内容请购买。
037 异柠檬酸盐作为钙离子活性缓冲剂在凝固反应中的应用
037 异柠檬酸盐作为钙离子活性缓冲剂在凝固反应中的应用李立英;许素菊
【期刊名称】《国际检验医学杂志》
【年(卷),期】2001(022)003
【摘要】无
【总页数】1页(P164)
【作者】李立英;许素菊
【作者单位】无
【正文语种】中文
【中图分类】R4
【相关文献】
1.用钙离子选择电极测量表面活性剂驱油体系中的钙离子浓度
2.单个核细胞促血浆凝固活性监测急性排斥反应的实验研究
3.凝固时间法测定血浆AT-Ⅲ活性及在肝病诊断中的临床应用
4.胶乳生物凝固中活性干菌种的凝固效果比较
5.Cl_2/TiCl_4体系引发异丁基乙烯基醚阳离子聚合的研究Ⅲ.聚合反应的影响因素及反应活性
因版权原因，仅展示原文概要，查看原文内容请购买。
苦参黄酮类化合物中GLUT4转运蛋白激动剂的虚拟筛选
苦参黄酮类化合物中GLUT4转运蛋白激动剂的虚拟筛选黄佩南;于雅楠;黄晓斌;李晓芝;陈锡欣;刘怡;陈磊;王淑美【期刊名称】《药学研究》【年(卷),期】2018(037)005【摘要】目的采用分子对接技术虚拟筛选苦参黄酮类化合物中葡萄糖转运蛋白4（GLUT4）转运蛋白激动剂。
方法搜集现已分离鉴定的128个苦参黄酮类化合物组成配体数据库,检索RCSB PDB数据库中葡萄糖转运蛋白4蛋白晶体结构并确定本研究用优势构象,以蛋白优势结构对应DrugBank中已上市的小分子药物平均打分为阈值,应用Discovery Studio 2.5（DS2.5）软件的CDOCKER模块进行分子对接。
结果虚拟筛选出打分高于阈值且排名前10%的化合物共12个并归纳了苦参黄酮作用靶点的主要活性位点,初步揭示了苦参黄酮抗糖尿病的作用机制。
结论基于分子对接的虚拟筛选可推断苦参黄酮化合物中促进葡萄糖转运蛋白4转运蛋白激动的有效成分,为进一步构效关系研究及研发基于新靶点的抗糖尿病类药物提供了一定的参考。
【总页数】5页(P249-252)【作者】黄佩南;于雅楠;黄晓斌;李晓芝;陈锡欣;刘怡;陈磊;王淑美【作者单位】[1]广东药科大学中药学院,广东广州510006;;[1]广东药科大学中药学院,广东广州510006;;[1]广东药科大学中药学院,广东广州510006;;[1]广东药科大学中药学院,广东广州510006;;[1]广东药科大学中药学院,广东广州510006;;[2]南方医科大学中医药学院,广东广州510515;;[1]广东药科大学中药学院,广东广州510006;[3]国家中医药管理局中药数字化质量评价技术重点研究室,广东广州510006;[4]广东省中药质量工程技术研究中心,广东广州510006;;[1]广东药科大学中药学院,广东广州510006;[3]国家中医药管理局中药数字化质量评价技术重点研究室,广东广州510006;[4]广东省中药质量工程技术研究中心,广东广州510006【正文语种】中文【中图分类】R284【相关文献】1.膳食因素和运动对脑内葡萄糖转运蛋白Glut1、Glut4基因表达的影响 [J], 魏守刚;褚金花;张淑华;肖忠新2.苦参黄酮类化合物中GLUT4转运蛋白激动剂的虚拟筛选 [J], 黄佩南;于雅楠;黄晓斌;李晓芝;陈锡欣;刘怡;陈磊;王淑美3.传统中药中抗动脉粥样硬化PPARα激动剂的虚拟筛选 [J], 杜霞;张鑫磊;李晔4.ppar-α激动剂的虚拟筛选研究 [J], 罗蓓;郭银应;陈双扣;任玉婷5.红藤化学成分中端粒酶TERT基因激动剂的虚拟筛选 [J], 汤建;徐滢滢;黄淑慧;刘梦;曹裕旻;闻崇炜因版权原因，仅展示原文概要，查看原文内容请购买。
反相高效液相色谱法测定人血浆中西米替丁浓度
反相高效液相色谱法测定人血浆中西米替丁浓度
陈季凤;程锦坤
【期刊名称】《皖南医学院学报》
【年(卷),期】1994(013)001
【摘要】在药物的生物利用度和药代动力学研究时,用比色法测定的专属性差,灵敏度低,现使用反相高效液相色谱法测定西米替丁的血液浓度,结果满意,现报告如下. 1 仪器、药品与试剂 Shimadzu LC-4A泵。
【总页数】2页(P79-80)
【作者】陈季凤;程锦坤
【作者单位】不详;不详
【正文语种】中文
【中图分类】R969.1
【相关文献】
1.反相高效液相色谱法测定人血浆中紫杉醇的浓度 [J], 陈小欢;许杜娟;夏泉;王欣晨;程钢;孙国平
2.反相高效液相色谱法测定人血浆中10-羟基卡马西平浓度 [J], 黄小芬;陈凤
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4.反相高效液相色谱法测定人血浆中兰索拉唑的浓度相关研究 [J], 谭姣章
5.反相高效液相色谱法测定人血浆中盐酸头孢替安的浓度 [J], 南志成
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