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1、Product Data SheetD-GalactoseCat. No.: HY-N0210CAS No.: 59-23-4分式: CHO分量: 180.16作靶点: Endogenous Metabolite作通路: Metabolic Enzyme/Protease储存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性数据体外实验 H2O : 100 mg/mL (555.06 mM; Need ultrasonic)DMSO : 50 mg/mL (277.53 mM; Need ultraso

2、nic)SolventMass1 mg 5 mg 10 mgConcentration制备储备液1 mM 5.5506 mL 27.7531 mL 55.5062 mL5 mM 1.1101 mL 5.5506 mL 11.1012 mL10 mM 0.5551 mL 2.7753 mL 5.5506 mL请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;旦配成溶液,请分装保存,避免反复冻融造成的产品失效。储备液的保存式和期限:-80C, 6 months; -20C, 1 month。-80C 储存时,请在 6 个内使,-20C 储存时,请在 1 个内使。体内实验请根据您的实验动物和给

3、药式选择适当的溶解案。以下溶解案都请先按照 In Vitro 式配制澄清的储备液,再依次添加助溶剂:为保证实验结果的可靠性,澄 的储备液可以根据储存条件,适当保存;体内实验的作液,建议您现现配,当天使; 以下溶剂前显的百分 指该溶剂在您配制终溶液中的体积占;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的式助溶1. 请依序添加每种溶剂: 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (13.88 mM); Clear solution此案可获得 2.5 mg/mL (13.88 mM,饱和度未知) 的澄

4、清溶液。以 1 mL 作液为例,取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 400 L PEG300 中,混合均匀;向上述体系中加50 L Tween-80,混合均匀;然后继续加 450 L 理盐定容 1 mL。2. 请依序添加每种溶剂: 10% DMSO 90% (20% SBE-CD in saline)Solubility: 2.5 mg/mL (13.88 mM); Clear solutionPage 1 of 2 www.MedChemE此案可获得 2.5 mg/mL (13.88 mM,饱和度未知) 的澄清溶液。以 1 mL 作液为例,取 100 L 25.

5、0 mg/mL 的澄 DMSO 储备液加到 900 L 20% 的 SBE-CD 理盐溶液中,混合均匀。3. 请依序添加每种溶剂: 10% DMSO 90% corn oilSolubility: 2.5 mg/mL (13.88 mM); Clear solution此案可获得 2.5 mg/mL (13.88 mM,饱和度未知) 的澄 溶液,此案不适于实验周 期在半个以上的实验。以 1 mL 作液为例,取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 900 L 油中,混合均匀。BIOLOGICAL ACTIVITY物活性 D-Galactose天然的糖,是葡萄糖的C-4差

6、向异构体。IC & Target Human Endogenous Metabolite体外研究 Galactose is important for the survival and virulence of bacteria. In Escherichia coli galactose is utilized by the Leloirpathway. Two anomers of d-galactose are used for different purposes, -d-galactose as a carbon source and -d-galactose for inducti

7、on of UDP-galactose synthesis for biosynthetic glycosylation1.体内研究 Chronic D-galactose exposure induces neurodegeneration by enhancing caspase-mediated apoptosis and inhibitingneurogenesis and neuron migration in mice, as well as increasing oxidative damage. In addition, D-galactose-induced toxicity

8、 in mice is a useful model for studying the mechanisms of neurodegeneration and neuroprotective drugs andagents2. D-galactose given by oral route causes cognitive impairments in rats which are accompanied by oxidativedamage. Cognitive impairments is observed in the open-field test in the 4th and 6th

9、 weeks after d-gal administration,as well as an impairment in spatial memory in the radial maze test after the 6th week of d-gal administration3.PROTOCOLAnimal Rats: D-galactose is dissolved in water for administration at the dose of 100 mg/kg of body weight, and given by oralAdministration 23 gavag

10、e, once a day, over a period of 1, 2, 4, 6 or 8 weeks. Animals are randomized into two groups: control animals(receiving water by oral gavage) or d-gal animals (receiving D-galactose by oral gavage). The behavioral tests andbiochemical analysis are undertaken on the1st, 2nd, 4th, 6th and 8th weeks a

11、fter the last administration of d-gal3.Mice: Male adult C57BL/6 mice are randomly divided into three groups (control, D-galactose, and D-galactose plus-LA). D-galactose (100 mg/kg) is injected subcutaneously (s.c.) daily into mice for 7 weeks. -LA (100 mg/kg bodyweight) is injected peritoneally (i.p

12、.) daily concomitantly for 7 weeks. All control animals are given saline2.MCE has not independently confirmed the accuracy of these methods. They are for reference only.户使本产品发表的科研献 PLoS Biol. 2018 Oct 18;16(10):e2006483.See more customer validations on HYPERLINK www.MedChemE www.MedChemEREFERENCESPa

13、ge 2 of 3 www.MedChemE1. Csiszovszki Z, et al. Structure and function of the D-galactose network in enterobacteria. MBio. 2011 Jun 28;2(4):e00053-11.2. Cui X, et al. Chronic systemic D-galactose exposure induces memory loss, neurodegeneration, and oxidativedamage in mice: protective effects of R-alpha-lipoic acid. J Neurosci Res. 2006 Aug 15;84(3):647-54.3. Budni J, et al. Oral administration of d-galactose induces cognitive impairments and oxidative damage in rats. Behav Brain Res. 2016 Apr 1;302:35-43.McePdfHeightCaut

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