Hesperetin belongs to the flavanone class of flavonoids. Hesperetin, in the form of its glycoside hesperidin, is the predominant flavonoid in lemons and oranges.
| 説明 | Hesperetin belongs to the flavanone class of flavonoids. Hesperetin, in the form of its glycoside hesperidin, is the predominant flavonoid in lemons and oranges. |
| In vitro | Hesperetin has the retention of antioxidant potential in self nano-emulsifying drug delivery system[1]. Hesperetin and NGR display broad-spectrum inhibition against human UGTs. In addition, Hesperetin exhibits strong inhibitory effects on UGT1A1, 1A3 and 1A9 (both IC50 and Ki values lower than 10 μM) and moderately inhibits UGT1A4, UGT1A7, UGT1A8 (IC50 values 29.68-63.87 μM)[2]. Hesperetin interacts with different types of proteins involving hydrogen bonds, pi-pi effects, pi-cation bonding and pi-sigma interactions with varying binding energies. Hesperetin exhibits drug-like properties which indicate its potential as a therapeutic option for CHIKV infection[3]. Hesperetin dose-dependently reduces GCDCA-induced caspase-3 activity in cultured primary rat hepatocytes. Hesperetin also dose-dependently reduces CM-induced Nos2 (iNOS) expression in hepatocytes. Interestingly, hesperetin-induced expression of the antioxidant gene haem oxygenase 1 (HO-1) about fourfold compared with cytokine mixture alone[5]. |
| In vivo | Preadministration of Hesperetin (40 mg/kg b.w., oral) markedly attenuates the Cd-induced oxidative stress and mitochondrial dysfunction, restores the antioxidant and membrane-bound enzyme activities and decreases apoptosis in the brain of rats[4]. Hesperetin (200 mg/kg) attenuates Con A-induced hepatocyte apoptosis and hepatic Nos2 (iNOS) expression in mice. In addition, Hesperetin co-treatment decreases the occurrence of apoptotic bodies, hydropic degeneration, nuclear fragments, autolysis and haemorrhage. The number of leukocytes infiltrated in liver tissue of mice with D-GalN/LPS-induced fulminant hepatitis are significantly decreased by hesperetin in a murine model[5]. |
| キナーゼ試験 | First, 0.5 mL tissue homogenate is diluted with 1 mL water. Then, to this mixture, 2.5 mL ethanol and 1.5 mL chloroform (all reagents chilled) are added and shaken for 1 min at 4°C, then centrifuged. The enzyme activity in the supernatant is determined. The assay mixture contained 1.2 mL sodium pyrophosphate buffer (0.025 M, pH 8.3), 0.1 mL 186 mM phenazine methosulfate (PMS), 0.3 mL 30 mM Nitroblue tetrazolium (NBT), and 0.2 mL of nicotinamide adenine dinucleotide (NADH), and appropriately diluted enzyme preparation and water in a total volume of 3 mL. Reaction is initiated by the addition of NADH. After incubation at 30°C for 90 min, the reaction is stopped by the addition of 1 mL glacial acetic acid. The reaction mixture is stirred vigorously and shaken with 4 mL n-butanol. The intensity of the chromogen in the butanol layer is measured at 560 nm against a butanol blank. A system without enzyme served as control. One unit of enzyme activity is defined as 50% inhibition of NBT reduction in 1 min under the assay conditions. |
| 植物由来 |
| 分子量 | 302.27 |
| 分子式 | C16H14O6 |
| CAS No. | 520-33-2 |
Powder: -20°C for 3 years
In solvent: -80°C for 2 years
Ethanol: <1 mg/mL
DMSO: 56 mg/mL (185.3 mM)
H2O: <1 mg/mL
( < 1 mg/ml refers to the product slightly soluble or insoluble )
参考文献
投与量変換You can also refer to dose conversion for different animals. 詳細
In vivo投与量計算 (透明溶液)計算器bottom
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Hesperetin 520-33-2 Apoptosis Autophagy GPCR/G Protein MAPK Neuroscience Stem Cells 5-HT Receptor p38 MAPK TGF-beta/Smad inhibit Inhibitor inhibitor
