Neosperidin dihydrochalcone - CAS 20702-77-6
Catalog number:
20702-77-6
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C28H36O15
Molecular Weight:
612.58
COA:
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Description:
Neohesperidin dihydrochalcone, is an artificial sweetener derived from citrus. The product is well known for having a strong synergistic effect when used in conjunction with other artificial sweeteners.
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Purity:
>98%
Synonyms:
NCI-c60764
MSDS:
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1.Neohesperidin dihydrochalcone down-regulates MyD88-dependent and -independent signaling by inhibiting endotoxin-induced trafficking of TLR4 to lipid rafts.
Xia X1, Fu J1, Song X1, Shi Q1, Su C1, Song E1, Song Y2. Free Radic Biol Med. 2015 Dec;89:522-32. doi: 10.1016/j.freeradbiomed.2015.08.023. Epub 2015 Oct 8.
Fulminant hepatic failure (FHF) is a lethal clinical syndrome characterized by the activation of macrophages and the increased production of inflammatory mediators. The purpose of this study was to investigate the effects of neohesperidin dihydrochalcone (NHDC), a widely-used low caloric artificial sweetener against FHF. An FHF experimental model was established in mice by intraperitoneal injection of D-galactosamine (d-GalN) (400mg/kg)/lipopolysaccharides (LPS) (10 μg/kg). Mice were orally administered NHDC for 6 continuous days and at 1h before d-GalN/LPS administration. RAW264.7 macrophages were used as an in vitro model. Cells were pre-treated with NHDC for 1h before stimulation with LPS (10 μg/ml) for 6h. d-GalN/LPS markedly increased the serum transaminase activities and levels of oxidative and inflammatory markers, which were significantly attenuated by NHDC. Mechanistic analysis indicated that NHDC inhibited LPS-induced myeloid differentiation factor 88 (MyD88) and TIR-containing adapter molecule (TRIF)-dependent signaling.
2.Neohesperidin Dihydrochalcone versus CCl₄-Induced Hepatic Injury through Different Mechanisms: The Implication of Free Radical Scavenging and Nrf2 Activation.
Su C1, Xia X1, Shi Q1, Song X1, Fu J1, Xiao C1, Chen H1, Lu B1, Sun Z1, Wu S1, Yang S1, Li X1, Ye X2, Song E1, Song Y1. J Agric Food Chem. 2015 Jun 10;63(22):5468-75. doi: 10.1021/acs.jafc.5b01750. Epub 2015 May 28.
Neohesperidin dihydrochalcone (NHDC), a sweetener derived from citrus, belongs to the family of bycyclic flavonoids dihydrochalcones. NHDC has been reported to act against CCl4-induced hepatic injury, but its mechanism is still unclear. We first discovered that NHDC showed a strong ability to scavenge free radicals. In addition, NHDC induces the phase II antioxidant enzymes heme oxygenase 1 (HO-1) and NAD(P)H/quinone oxidoreductase 1 (NQO1) through the activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/antioxidant response element (ARE) signaling. Further assays demonstrated that NHDC induces accumulation of Nrf2 in the nucleus and augmented Nrf2-ARE binding activity. Moreover, NHDC inhibits the ubiquitination of Nrf2 and suggests the modification of Kelch-like ECH-associated protein 1 (Keap1) and the disruption of the Keap1/Nrf2 complex. c-Jun N-terminal kinase (JNK) and p38 but not extracellular signal-regulated protein kinase (ERK) phosphorylations were up-regulated by NHDC treatment.
3.Artificial sweetener neohesperidin dihydrochalcone showed antioxidative, anti-inflammatory and anti-apoptosis effects against paraquat-induced liver injury in mice.
Shi Q1, Song X1, Fu J1, Su C1, Xia X1, Song E1, Song Y2. Int Immunopharmacol. 2015 Dec;29(2):722-9. doi: 10.1016/j.intimp.2015.09.003. Epub 2015 Sep 9.
The present study evaluated the protective effect of artificial sweetener neohesperidin dihydrochalcone (NHDC) against paraquat (PQ)-induced acute liver injury in mice. A single dose of PQ (75mg/kg body weight, i.p.) induced acute liver toxicity with the evidences of increased liver damage biomarkers, aspartate transaminase (AST) and alanine transaminase (ALT) activities in serum. Consistently, PQ decreased the antioxidant capacity by reducing glutathione peroxidase (GP-X), glutathione-S-transferase (GST) and catalase (CAT) activities, glutathione (GSH) level and total antioxidant capacity (T-AOC), as well as increasing reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS) levels. Histopathological examination revealed that PQ induced numerous changes in the liver tissues. Immunochemical staining assay indicated the upregulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions.
4.Effect of neohesperidin dihydrochalcone on the activity and stability of alpha-amylase: a comparative study on bacterial, fungal, and mammalian enzymes.
Kashani-Amin E1,2, Ebrahim-Habibi A1,2, Larijani B2, Moosavi-Movahedi AA3. J Mol Recognit. 2015 Oct;28(10):605-13. doi: 10.1002/jmr.2473. Epub 2015 Mar 25.
Neohesperidin dihydrochalcone (NHDC) was recently introduced as an activator of mammalian alpha-amylase. In the current study, the effect of NHDC has been investigated on bacterial and fungal alpha-amylases. Enzyme assays and kinetic analysis demonstrated the capability of NHDC to significantly activate both tested alpha-amylases. The ligand activation pattern was found to be more similar between the fungal and mammalian enzyme in comparison with the bacterial one. Further, thermostability experiments indicated a stability increase in the presence of NHDC for the bacterial enzyme. In silico (docking) test locates a putative binding site for NHDC on alpha-amylase surface in domain B. This domain shows differences in various alpha-amylase types, and the different behavior of the ligand toward the studied enzymes may be attributed to this fact.
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CAS 20702-77-6 Neosperidin dihydrochalcone

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