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1、Product Data SheetNaringeninCat. No.: HY-N0100CAS No.: 480-41-1分式: CHO分量: 272.25作靶点: PPAR; Reactive Oxygen Species; Influenza Virus; Endogenous Metabolite作通路: Cell Cycle/DNA Damage; Immunology/Inflammation; MetabolicEnzyme/Protease; NF-B; Anti-infection储存式: Powder -20C 3 years4C 2 yearsIn solvent -8

2、0C 6 months-20C 1 month溶解性数据体外实验 DMSO : 50 mg/mL (183.65 mM)* means soluble, but saturation unknown.SolventMass1 mg 5 mg 10 mgConcentration制备储备液1 mM 3.6731 mL 18.3655 mL 36.7309 mL5 mM 0.7346 mL 3.6731 mL 7.3462 mL10 mM 0.3673 mL 1.8365 mL 3.6731 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

3、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-8

4、0 45% salineSolubility: 3 mg/mL (11.02 mM); Clear solution此案可获得 3 mg/mL (11.02 mM,饱和度未知) 的澄清溶液。以 1 mL 作液为例,取 100 L 30.0 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: 3 mg/mL (11.02 mM); Clear solut

5、ionPage 1 of 2 www.MedChemE此案可获得 3 mg/mL (11.02 mM,饱和度未知) 的澄清溶液。以 1 mL 作液为例,取 100 L 30.0 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: 3 mg/mL (11.02 mM); Clear solution此案可获得 3 mg/mL (11.02 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 30.0

6、 mg/mL 的澄 DMSO 储备液加到 900 L 油中,混合均匀。BIOLOGICAL ACTIVITY物活性 Naringenin葡萄柚中主 的 烷酮; 显出强烈的抗炎和抗氧化活性。Naringenin 具有抗登热病毒 (DENV) 活性。IC & Target Human Endogenous Metabolite(批量添加)体外研究 Naringenin is shown to inhibit the proliferation of HepG2 cells resulted partly from an accumulation of cells in theG0/G1 and G

7、2/M phase of the cell cycle. Naringenin has been shown to induce apoptosis as evidenced by nucleidamage and increased proportion of apoptotic cells. Naringenin triggers the mitochondrial-mediated apoptosispathway as shown by an increased ratio of Bax/Bcl-2, subsequent release of cytochrome C, and se

8、quential activationof caspase-31. Naringenin exposure significantly reduces the cell viability of A431 cells with a concomitant increasein nuclear condensation and DNA fragmentation in a dose dependent manner. Cell cycle study shows that naringenininduced cell cycle arrest in G0/G1 phase of cell cyc

9、le and caspase-3 analysis reveal a dose dependent increment incaspase-3 activity which leads to cell apoptosis2.体内研究 Naringenin supplementation causes a significant reduction in the amount of total triglyceride and cholesterol inplasma and liver. In addition, naringenin supplementation lowers adipos

10、ity and triglyceride contents in parametrialadipose tissue. Naringenin-fed animals show a significant increase in PPAR protein expression in the liver. Theexpression of CPT-1 and UCP2, known to be regulated by PPAR, is markedly enhanced by naringenin treatment3.Naringenin increases hepatic fatty aci

11、d oxidation through a PPAR coactivator 1/PPAR-mediated transcriptionprogram. It prevents sterol regulatory element-binding protein 1cmediated lipogenesis in both liver and muscle byreducing fasting hyperinsulinemia. Naringenin decreases hepatic cholesterol and cholesterol ester synthesis4.Naringenin

12、 inhibits TNF-induced VSMC proliferation and migration in a dose-dependent manner. Mechanisticstudy demonstrates that naringenin prevents ERK/MAPK and Akt phosphorylation while left p38 MAPK and JNKunchanged. Naringenin also blocks the increase of ROS generation induced by TNF-5.PROTOCOLCell Assay 1

13、 Naringenin is dissolved in DMSO and diluted in cell culture medium. The cells are rinsed with PBS and grown in amedium containing various concentrations of naringenin (50, 100, 150, 200, 250, 300 M). The solvent DMSO treatedcells are served as control. After 24 hrs of treatment, the medium is remov

14、ed and replaced by another mediumcontaining MTT. Cell viability is measured using the MTT assay1.MCE has not independently confirmed the accuracy of these methods. They are for reference only.Animal Rats: Semi-purified, powdered diets are prepared for concentrations of naringenin: 0, 0.003, 0.006, a

15、nd 0.012% ofAdministration 34 diet. After 7 days of acclimatization, rats are assigned to one of four groups, with six animals per group, and fedsemi-purified experimental diets for 6 weeks. The experimental diets contain 16% fat, 45.5% sucrose, and differentnaringenin concentration (0, 0.003, 0.006

16、, or 0.012%) (Table 1). Rats have ad libitum access to food and water duringPage 2 of 3 www.MedChemEthe study period. Food intake and body weight are measured throughout the experiment3.Mouse: Eight- to 12-week-old mice are fed ad libitum a rodent standard diet or a high-fat diet containing 42% ofca

17、lories from fat plus cholesterol (0.05% wt/wt). Naringenin is added to the Western diet at 1 or 3% (wt/wt). Ldlr/mice are fed for 4 weeks and C57BL/6J mice for 30 weeks. Food intake is measured daily, and body weight ismeasured biweekly. Mice are fasted for 6 h before intervention4.MCE has not indep

18、endently confirmed the accuracy of these methods. They are for reference only.户使本产品发表的科研献 Biochem Biophys Res Commun. 2018 Sep 3;503(1):297-303. Int J Insect Sci. 2018 Feb 28;10:1179543318758409.See more customer validations on HYPERLINK www.MedChemE www.MedChemEREFERENCES1. Arul D, et al. Naringeni

19、n (citrus flavonone) induces growth inhibition, cell cycle arrest and apoptosis in human hepatocellular carcinoma cells. PatholOncol Res. 2013 Oct;19(4):763-70.2. Ahamad MS, et al. Induction of apoptosis and antiproliferative activity of naringenin in human epidermoid carcinomacell through ROS gener

20、ation andcell cycle arrest. PLoS One. 2014 Oct 16;9(10):e110003.3. Cho KW, et al. Dietary naringenin increases hepatic peroxisome proliferators-activated receptor proteinexpression and decreases plasma triglycerideand adiposity in rats. Eur J Nutr. 2011 Mar;50(2):81-8.4. Mulvihill EE, et al. Naringenin prevents dyslipidem

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