1. MAPK/ERK Pathway
    Apoptosis
  2. p38 MAPK
    Apoptosis
  3. Hesperetin

Hesperetin 

Cat. No.: HY-N0168 Purity: 98.04%
Handling Instructions

Hesperetin is a natural flavanone, and acts as a potent and broad-spectrum inhibitor against human UGT activity. Hesperetin induces apoptosis via p38 MAPK activation.

For research use only. We do not sell to patients.

Hesperetin Chemical Structure

Hesperetin Chemical Structure

CAS No. : 520-33-2

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10 mM * 1 mL in DMSO USD 66 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 6 publication(s) in Google Scholar

Top Publications Citing Use of Products

    Hesperetin purchased from MCE. Usage Cited in: Nutr Cancer. 2019 Jul 11:1-8.

    U-251 cells are cultured with indicated concentration of Hesperetin for 24 h. Then the cells are stained with DAPI and observed under a fluorescence microscope.

    Hesperetin purchased from MCE. Usage Cited in: Nutr Cancer. 2019 Jul 11:1-8.

    The expression of Bax and Bcl-2 was examined by western blotting. GAPDH was served as a loading control.

    Hesperetin purchased from MCE. Usage Cited in: Nutr Cancer. 2019 Jul 11:1-8.

    Hesperetin induced G2/M arrest in GBM cell. Cells are treated with vehicle or various doses of hesperetin for 24 h. Whole cell lysates are immunoblotted with indicated antibodies. The protein levels of p21, CDK1, and cyclin B1 are measured by western blotting.

    Hesperetin purchased from MCE. Usage Cited in: Nutr Cancer. 2019 Jul 11:1-8.

    p38 MAPK activation is involved in Hesperetin-induced apoptosis. The phosphorylation of p38 MAPK, JNK, and ERK in U-21 cells treated with hesperetin is analyzed by western blotting.
    • Biological Activity

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    Description

    Hesperetin is a natural flavanone, and acts as a potent and broad-spectrum inhibitor against human UGT activity. Hesperetin induces apoptosis via p38 MAPK activation.

    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. Besides, 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 projects 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) significantly 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. Hesperetin co-treatment also 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].

    Molecular Weight

    302.28

    Formula

    C₁₆H₁₄O₆

    CAS No.

    520-33-2

    SMILES

    O=C1C[[email protected]@H](C2=CC=C(OC)C(O)=C2)OC3=CC(O)=CC(O)=C13

    Shipping

    Room temperature in continental US; may vary elsewhere

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 33 mg/mL (109.17 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 3.3082 mL 16.5410 mL 33.0819 mL
    5 mM 0.6616 mL 3.3082 mL 6.6164 mL
    10 mM 0.3308 mL 1.6541 mL 3.3082 mL
    *Please refer to the solubility information to select the appropriate solvent.
    References
    Kinase Assay
    [4]

    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.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [4]

    After 7 days of adjusting, the animals are randomly divided into 10 experimental groups. Control group (n=8): These animals are treated with the equivalent volume of PBS as used for the administration of Con A and D-GalN/LPS. Control hesperetin group (n=8): The mice are treated with hesperetin 400 mg/kg p.o. in 0.5% sodium carboxymethylcellulose (CMC-Na) solution for 10 days. Con A group (n=15): The animals are treated with the same volume of CMC-Na as used for administration of hesperetin for 10 days and are challenged with Con A (i.v.15 mg/kg). Con A + hesperetin groups: The animals receive various doses of hesperetin (100, 200, 400 mg/kg) p.o. for 10 days before Con A injection (each group n=15). D-GalN/LPS group (n=15): The animals are given CMC-Na for 10 days and injected i.p. with D-GalN (700 mg/kg)/LPS (5 μg/kg). D-GalN/LPS + hesperetin groups: Three doses of hesperetin (100, 200, 400 mg/kg) are given to mice once daily for 10 days. D-GalN (700 mg/kg)/LPS (5 μg/kg) are injected i.p. (each group n=15).

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References
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