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8-Epidiosbulbin E acetate


CAS No. : 91095-48-6

91095-48-6
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Cat. No. : HY-N7047
M.Wt: 388.41
Formula: C21H24O7
Purity: >98 %
Solubility: DMSO : 100 mg/mL (ultrasonic)
Introduction of 91095-48-6 :

8-Epidiosbulbin E acetate, a furanoid, is abundant in Dioscorea bulbifera L.. 8-Epidiosbulbin E acetate exhibits broad-spectrum plasmid-curing activity against multidrug-resistant (MDR) bacteria. 8-Epidiosbulbin E acetate induces liver injury in mice[1][2]. In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

8-Epidiosbulbin E acetate can be used in animal modeling to create liver injury models. Pre-treatment with Ketoconazole (KTC) prevents liver injury caused by 8-Epidiosbulbin E acetate and increases the Cmax and AUC of 8-Epidiosbulbin E acetate in plasma by 7-fold and 13-fold, respectively, while reducing the urinary excretion of glutathione (GSH) conjugates derived from 8-Epidiosbulbin E acetate[1][2].

Induction of liver deseases[1][2].
Background
8-Epidiosbulbin E acetate was hepatotoxic and the electrophilic intermediate generated by its metabolic activation of the furan ring mediated by cytochromes P450 was responsible for 8-Epidiosbulbin E acetate-induced liver injury[1].
8-Epidiosbulbin E acetate mainly damaged hepatic cells through the aberrant regulation of multiple systems primarily including bile acid metabolism, and taurine and hypotaurine metabolism. In addition, an imbalance of bile acid metabolism was found to play a key pat in response to 8-Epidiosbulbin E acetate-triggered hepatotoxicity[2].
Specific Modeling Methods
Mice: Kun-Ming• male• weighing 17-20 g[1]
Administration: 50-150 mg/kg• i.p.• a single dose for 12, 24, 36, and 48 h[1]
Mice: ICR• male• 4-5 weeks of age• weighing: 18-22 g[2]
Administration: 150 mg/kg•p.o.•a single dose for 36 h[2]
Note
(1) Mice had free access to food and water and were housed in a temperature-controlled (22±4 °C) facility with a 12 h dark/light cycle for at least 5 or 7 days before treatment. The animals were sacrificed 12, 24, 36, and 48 h after the treatment[1][2].
(2) 8-Epidiosbulbin E acetate (100 mg) was individually suspended in 10 mL of corn oil[1].
(3) 8-Epidiosbulbin E acetate was suspended in 0.5% CMC-Na[2].
Modeling Indicators
Molecular changes: 8-Epidiosbulbin E acetate administration increased the serum ALT, AST, TBIL and DBIL levels in a time- and dose-dependent manner[1][2].
Pathology change: 8-Epidiosbulbin E acetate administration showed inflammatory cell infiltration, hepatic cell necrosis and focal necrosis in mice[2].
Metabolic change: 8-Epidiosbulbin E acetate administration elevated phenylalanine, tyrosine and tryptophan biosynthesis. Moreover, several other important pathways, including citrate cycle (TCA cycle), phenylalanine metabolism, β-alanine metabolism and taurine and hypotaurine metabolism, were activated in both serum and livers[2].
Correlated Product(s): Buthionine sulfoximine (HY-106376)
Opposite Product(s): Ketoconazole (HY-B0105)

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