丙二酸2-氨基-1-乙酯置于盐酸体系中,用 水 作为反应溶剂,化学反应 8.0H,反应生成 甲酰氨基丙二酸二乙酯
参考文献:Peroxisome Proliferator-Activated Receptor-γ Mediates The Anti-Inflammatory Effect Of 3-Hydroxy-4-Pyridinecarboxylic Acid Derivatives: Synthesis And Biological Evaluation
标题:Peroxisome Proliferator-Activated Receptor-γ Mediates The Anti-Inflammatory Effect Of 3-Hydroxy-4-Pyridinecarboxylic Acid Derivatives: Synthesis And Biological Evaluation
摘要:Seven 3-Hydroxy-4-Pyridinecarboxylic Acid Derivatives (Hps),Aza-Analogues Of Salicylic Acid And Structurally Close To Other Potent Inflammatory Pyridine Compounds Such As Aminopyridinylmethanols And Aminopyridinamines,Were Synthesized,And Their Anti-Inflammatory Activity Was Evaluated. The Synthesis Was Performed By Adopting A General Procedure Involving An Intramolecular Diels-Alder Cycloaddition Of Oxazoles With Acrylic Acid To Form Various Substituted Pyridinic Acids. The Newly Synthesized Hps Did Not Exhibit Cytotoxic Activity On Human Monocytes-Derived Macrophages At Concentrations Up To 10(2) Mu M. Anti-Inflammatory Activity Of The Compounds Was Screened In Vitro By Evaluating The Capability To Inhibit Cytokines Release From Lipopolysaccharide (Lps) Stimulated Human Macrophages. 3-Hydroxy-1-Methyl-4-Pyridinecarboxylic Acid (24) Was Found To Be The Most Active Hp. At 10 Mu M Concentration,Hp 24 Reduced Lps-Induced And Nuclear Factor-Kappa B Activation And Cyclooxygenase-2 Expression,While Increased Intracellular Reactive Oxygen Species Generation And Peroxisome Proliferator-Activated Receptor (Ppar-Gamma) Mrna Transcript Level. Indeed,Pre-Treatment Of Lps-Exposed Human Macrophages With Ppar-Gamma Specific Antagonist Completely Prevented Hp 24-Induced Tnf-Alpha And Il8 Down Regulation,Demonstrating That The Ppar Gamma Pathway Is Mandatory For The Hp 24 Anti-Inflammatory Effect. Finally,Daily Treatment With Hp 24 Ameliorated The Outcome Of Dss-Induced Colitis In Mice,Significantly Reducing Colonic Mpo Activity And Il-1 Beta Tissue Levels. (C) 2013 Elsevier Masson Sas. All Rights Reserved.
DOI:10.1016/j.Ejmech.2013.01.024