CAS No. : 50-22-6
(Synonyms: 17-Deoxycortisol; 11β,21-Dihydroxyprogesterone; Kendall's compound B)
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| Cat. No. : | HY-B1618 |
| M.Wt: | 346.47 |
| Formula: | C21H30O4 |
| Purity: | >98 % |
| Solubility: | Ethanol : 14.29 mg/mL (ultrasonic);H2O : < 0.1 mg/mL (ultrasonic);DMSO : 100 mg/mL (ultrasonic) |
Corticosterone (17-Deoxycortisol) is an orally active and adrenal cortex-produced glucocorticoid, which plays an important role in regulating neuronal functions of the limbic system (including hippocampus, prefrontal cortex, and amygdala). Corticosterone increases the Rab-mediated AMPAR membrane traffic via SGK-induced phosphorylation of GDI. Corticosterone also interferes with the maturation of dendritic cells and shows a good immunosuppressive effect[1][2][3][4].
In Vitro: Corticosterone (100 nM; 30 min) via SGK phosphorylation of GDI at Ser-213, increases the formation of GDI-Rab4 complex, facilitating the functional cycle of Rab4 and Rab4-mediated recycling of AMPARs to the synaptic membrane[1].
Corticosterone (CORT) (1 µM; 48 h) shows good immunosuppressive properties (functionally compromises maturation of BMDC), which impairs LPS-induced up-regulation of maturation-associated markers (MHC class II, B7.2, B7.1 and CD40)[2].
In Vivo: Corticosterone results in a marked reduction in the ability of BMDC cells to prime naive CD8+ T cells in vivo[2].
Corticosterone (0.03 or 1 mg/kg; s.c.; single) downregulates expression of BDNF mRNA in dentate gyrus and CA1 of rats[3].
Corticosterone (2.6 mg/kg; in animal feedings; 8 days) restores ethanol intake and preference to approximately normal preoperative levels in adrenalectomy (ADX) rats[4].
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