Hydrocortisone

SKU: orb1308010

Description

Hydrocortisone (Cortisol) is a glucocorticoid hormone secreted by the adrenocortex. Hydrocortisone agonizes the glucocorticoid receptor, which promotes proteolytic metabolism, gluconeogenesis, capillary wall stabilization, and renal calcium excretion, as well as suppressing immune and inflammatory responses.

Research Area

Metabolism Research

Key Properties

• CAS Number: 50-23-7
• MW: 362.46
• Purity: 99.95%
• Formula: C₂₁H₃₀O₅
• SMILES: C[C@@]12[C@]([C@]3([C@@]([C@]4(C)C(CC3)=CC(=O)CC4)([C@@H](O)C1)[H])[H])(CC[C@@]2(C(CO)=O)O)[H]
• Target: Endogenous Metabolite,Glucocorticoid Receptor
• Solubility: DMSO: 127.5 mg/mL (351.76 mM), Sonication is recommended. Ethanol: 22 mg/mL (60.7 mM), Sonication is recommended.

Bioactivity

• Target IC50:
  LTC4:3.6 nM|PGD2:480 nM|IFN-γ (Equine):0.086 μM|NF-κB:15.52 nM|PGE2:750 nM|GR:91 nM (Ki)
• In Vivo:
  In ex vivo guinea pig hearts, Hydrocortisone reduces post-ischemic oxidative stress, perfusion pressure, and effusion formation. Withi the human cerebral microvascular endothelial cell line hCMEC/D3, Hydrocortisone prevents endothelial barrier disruption induced by pro-inflammatory stimulation (administration of TNFα), partly by maintaining occludin levels. Hydrocortisone induces class-switch recombination from Sμ to Sε in IL-4-treated B cells, supporting a model for sequential isotype transformation from IgM to IgE through IgG4. Following dendritic cell treatment, Hydrocortisone decrease the expression of MHC class II molecules the dendritic-specific marker CD83, and costimulatory molecule CD86, while significantly reducing IL-12 secretion. Additionally, it inhibit the increase of IL-4 (induced by IFN-γ) but does not affect IL-5. Hydrocortisone lowers T cell proliferation in dendritic cells. It prevents TNF-α-induced severe degradation of glycocalyx, increases in coronary resistance, vascular leakage and permeability, hydroxyethyl starch, and causes degranulation of mast cells in ex vivo guinea pig hearts. Hydrocortisone inhibit the shedding of multili and glycosaminoglycans-1, heparan sulfate, and hyaluronic acid post-ischemia and suppresse the release of histamine from resident mast cells.
• In Vitro:
  METHODS: Human articular chondrocytes were cultured in medium containing Hydrocortisone (0.05-1.0 μg/ml), an the relevant indexes were measured by Flow Cytometry. Results the catabolic signaling pathway of chondrocytes treated with 0.05 μg mL Hydrocortisone was reduced, an the ability to synthesize ECM macromolecules was enhanced. METHODS: Porcine brain capillary endothelial cells PBCEC were cultured with medium containing Hydrocortisone (550 nM) for seven days, an the cytoskeleton was examined using fluorescence microscopy. Results: Hydrocortisone-induced cytoskeletal rearrangement.
• Cell Research:
  Cells are plated on top of collagen IV-coated transwell chambers for six-well plates (24 mM diameter, membrane material: polyethylene terephthalate (PET), 0.4 μM pores, pore density 1. × 06 cm2) at densities of 2. × 04 cells cm2 per well. When they have reached confluence At day 5 the different Experimental sets of cells are transferred to differentiation medium containing reduced amounts of FCS and treated with TNFα or hydrocortisone as indicated.

Storage & Handling

• Storage: keep away from direct sunlight | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Disclaimer: For research use only

Alternative Names

Cortisol, Endogenous Metabolite, Hydrocortisone, Glucocorticoid Receptor, GlucocorticoidReceptor, EndogenousMetabolite, Inhibitor, inhibit

Compound Identifiers

PubChem CID

5754