product name 20-Hydroxyecdysone
Description: 20-Hydroxyecdysone (also known as B-ecdysone, Commisterone Ecdysterone, 20E) is a naturally occurring ecdysteroid hormone which controls the ecdysis (moulting) and metamorphosis of arthropods. In H4IIE cell culture, 20-Hydroxyecdysone treatment decreases expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), reduces glucose production, and induces Akt2 phosphorylation sensitive to the phosphoinositide-3 kinase pathway-specific inhibitor LY-294002. 20-Hydroxyecdysone treatment before or after CoCl2 exposure significantly ameliorates CoCl2-induced cellular injuries.
References: Arch Insect Biochem Physiol. 2012 Apr;79(4-5):207-19; J Cell Biochem. 2010 Dec 15;111(6):1512-21; Am J Physiol Endocrinol Metab. 2009 Mar;296(3):E433-9.
480.63
Formula
C27H44O7
CAS No.
5289-74-7
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 96 mg/mL (199.7 mM)
Water: <1 mg/mL
Ethanol: 96 mg/mL (199.7 mM)
Solubility (In vivo)
1% DMSO+30% polyethylene glycol+1% Tween 80: 30 mg/mL
Synonyms
B-ecdysone,Commisterone
other peoduct :
In Vitro |
In vitro activity: In H4IIE cell culture, 20-Hydroxyecdysone treatment decreases expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), reduces glucose production, and induces Akt2 phosphorylation sensitive to the phosphoinositide-3 kinase pathway-specific inhibitor LY-294002. 20-Hydroxyecdysone treatment before or after CoCl2 exposure significantly ameliorates CoCl2-induced cellular injuries. 20-Hydroxyecdysone dramatically reduces the CoCl2-induced production of reactive oxygen species (ROS), decreases the depolarization of the mitochondrial membrane, inhibits the release of cytochrome c into the cytosol, increases the Bax/Bcl-2 ratio, and eliminates the CoCl2-induced activation of caspase-3. 20-Hydroxyecdysone inhibits NF-κB activation in HeLa cells stably transfected with an IL-6-bound reporter gene with IC50 of 31.8 µM. In vitro treatment of larval fat body tissues with 20-Hydroxyecdysone upregulates the apoptotic genes including Apaf-1, Nedd2 like1, Nedd2 like2, ICE1, ICE3, ICE5, Arp, and IAP. 20-Hydroxyecdysone reverses TGF-β1-induced increase in intracellular and extracellular fibronectin, and reverses TGF-β1-induced down-regulation of Smad7. Additionally, 20-Hydroxyecdysone significantly attenuates TGF-β1-induced upregulation of Smad2/3 and pSmad2/3, and downregulation of E-Cadherin. Moreover, 20-Hydroxyecdysone dramatically suppresses TGF-β1-induced increases in the expression of Snail. Kinase Assay: Cell Assay: |
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In Vivo | Oral administration of 20-Hydroxyecdysone (10 mg/kg/day for 13 weeks) ameliorates obesity and insulin resistance in C57BL/6J mice fed a high-fat diet and produces a significant decrease of body weight gain and body fat mass compared with untreated animals. In addition, plasma insulin levels and glucose tolerance are significantly lowered by 20-Hydroxyecdysone treatment. These changes are accompanied by the reduced hepatic expression of PEPCK and G6Pase and increased adiponectin production by visceral fat tissue. In the fat body of the silkworm, Bombyx mori, injection of 20-Hydroxyecdysone into day 2 of fifth instar larvae significantly induces apoptosis and upregulates apoptotic genes after 6 hours of treatment. 20-Hydroxyecdysone (5 mg/kg/day) treatment does not have potent anabolic properties, however, a muscle-specific increase is observed and genes are identified to provide an explanation for the muscle accretion. |
Animal model | Male C57BL/6J mice fed a high-fat diet |
Formulation & Dosage | Formulated in vehicle solution (10% DMSO in corn oil); 10 mg/kg/day; Oral administration |
References | Arch Insect Biochem Physiol. 2012 Apr;79(4-5):207-19; J Cell Biochem. 2010 Dec 15;111(6):1512-21; Am J Physiol Endocrinol Metab. 2009 Mar;296(3):E433-9. |