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Glycyrrhizic Acid (glycyrrhizic + acid)
Selected AbstractsPreparation of Glycyrrhizic Acid (I) and Its Practically Useful Salts from the Commercial Licorice Roots Extract.CHEMINFORM, Issue 30 2005R. M. Kondratenko No abstract is available for this article. [source] Carbenoxolone and mefloquine suppress tremor in the harmaline mouse model of essential tremorMOVEMENT DISORDERS, Issue 10 2006Fredricka C. Martin PhD Abstract Excessive olivo-cerebellar synchrony is implicated in essential tremor. Because synchrony in some networks is mediated by gap junctions, we examined whether the gap junction blockers heptanol, octanol, carbenoxolone, and mefloquine suppress tremor in the mouse harmaline model, and performed an open-treatment clinical study of mefloquine for essential tremor. Digitized motion was used to quantify tremor in mice administered harmaline, 20 mg/kg s.c. In mice the broad-spectrum gap junction blockers heptanol, octanol (350 mg/kg i.p. each), and carbenoxolone (20 mg/kg) suppressed harmaline tremor. Mefloquine (50 mg/kg), which blocks gap junctions containing connexin 36, robustly suppressed harmaline tremor. Glycyrrhizic acid (related to carbenoxolone) and chloroquine (related to mefloquine), which do not block gap junctions, failed to suppress harmaline tremor in mice. Clinically, tremor was assessed with standard rating scales, and subjects asked to take 62.5, 125, and 250 mg mefloquine weekly for 12 weeks at each dose. None of the four human subjects showed a meaningful tremor reduction with mefloquine, likely because clinical levels were below those required for efficacy. In view of recent genetic evidence, the anti-tremor mechanism of these compounds is uncertain but may represent a novel therapeutic target, possibly involving gap junctions other than those containing connexin 36. © 2006 Movement Disorder Society [source] Discovery and design of novel inhibitors of botulinus neurotoxin A: targeted ,hinge' peptide librariesJOURNAL OF APPLIED TOXICOLOGY, Issue 1 2003J. Hayden Abstract Intoxication by the zinc protease botulinus neurotoxin A (BoNT-A) results from cleavage of a single Q,R bond in the neuronal protein SNAP-25, which disables the docking mechanism required for neurotransmitter release. In the present study, potential inhibitors of BoNT-A were assessed from their effects on the BoNT-A cleavage of a synthetic 17-mer peptide (SNAP-25, residues 187,203) spanning the Q,R cleavage site. Compounds that inhibited BoNT-A included thiols (zinc chelators) such as dithiothreitol, dimercaptopropanesulfonic acid, mercaptosuccinic acid and captopril. In addition, compounds containing multiple acidic functions, such as the SNARE motif V2 (ELDDRADALQ), the tripeptide Glu-Glu-Glu and the steroid glycoside glycyrrhizic acid, were effective inhibitors. ,Hinge' peptide mini-libraries (PMLs) having the structure acetyl-X1 -X2 -linker-X3 -X4 -NH2 or X1 -X2 -linker-X3, where X1,X4 were mixtures of selected amino acids and the flexible linker was 4-aminobutyric acid, also provided effective inhibition. Targeted PMLs containing the acidic amino acids Asp and Glu, the scissile-bond amino acids Gln and Arg and the zinc chelators His and Cys produced pronounced inhibition of BoNT-A. Deconvolution of these libraries will provide novel ligands with improved inhibitory potency as leads in the design of peptide mimetics to treat BoNT poisoning. Copyright ? 2003 Crown in the right of Canada. Published by John Wiley and Sons, Ltd. [source] Concentration and separation of glycyrrhizic acid by foam separationJOURNAL OF CHEMICAL TECHNOLOGY & BIOTECHNOLOGY, Issue 6 2002Jun-Gang Ma Abstract By the aid of the surface activities of glycyrrhizic acid, foam separation can be used to extract and concentrate it. The effects of operating parameters such as flow rate of air, initial feed concentration, pH and ionic strength on the enrichment ratio and recovery yield of glycyrrhizic acid are investigated in detail. In addition, the influences of other surface-active substances in solution, such as proteins, on the separation of glycyrrhizic acid are also discussed. The experimental results show that foam separation is a simple and effective method to separate and concentrate glycyrrhizic acid. © 2002 Society of Chemical Industry [source] Azathioprine hepatotoxicity and the protective effect of liquorice and glycyrrhizic acidPHYTOTHERAPY RESEARCH, Issue 8 2006Yue-Ting Wu Abstract This study aimed to evaluate the responses of human hepatocytes to azathioprine hepatotoxicity in comparison with the well-studied azathioprine hepatotoxicity in rat hepatocytes and the effects of protective agents to suppress azathioprine hepatotoxicity. Azathioprine presented its hepatotoxicity at clinically relevant concentrations (lower than 10 µm) in primary rat hepatocytes after 48 h of treatment as shown by a severe decrease in cell viability as well as intracellular GSH depletion. However, primary human hepatocytes exhibited only significant intracellular GSH depletion after treatment with azathioprine at these clinically relevant concentrations, while a reduction in cell viability by 29% was only evidenced after 48 h of treatment with azathioprine at the high concentration of 50 µm. In addition, a monolayer culture of primary rat hepatocytes was used as an in vitro model to examine the protective effects of antihepatotoxic drugs including glutathione (GSH), N-acetylcysteine (NAC, a GSH precursor), liquorice and glycyrrhizic acid (GA), a major bioactive component of liquorice, against hepatotoxicity of 1 µm azathioprine. It was found that both liquorice and GA showed substantial protection according to assays of cell viability and intracellular GSH, while neither GSH nor NAC had such a protective function. Similarly, GA protected human hepatocytes from intracellular GSH depletion on exposure to 1 µm azathioprine. These results implied that GA or liquorice could be considered as potent protection agents against azathioprine hepatotoxicity. Copyright © 2006 John Wiley & Sons, Ltd. [source] | |||||||||||||