product name Dexamethasone (DHAP)
Description: Dexamethasone (also known as DHAP) is a potent synthetic member of the glucocorticoid class of steroid drugs, and an interleukin receptor modulator that has anti-inflammatory and immunosuppressant effects. Dexamethasone has anti-inflammatory and immunosuppressant effects. It is 25-fold more potent than cortisol in its glucocorticoid effect, while having minimal mineralocorticoid effect. Dexamethasone is used for the treatment of many conditions including: rheumatologic problems, a number of skin diseases such as erythema multiforme, severe allergies, asthma etc.
References: Neurosci Lett. 2003 Jun 26;344(2):112-6; J Physiol. 2003 Feb 15;547(Pt 1):61-6.
392.46
Formula
C22H29FO5
CAS No.
50-02-2
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 79 mg/mL (201.3 mM)
Water: <1 mg/mL
Ethanol: 6 mg/mL (15.3 mM)
Solubility (In vivo)
30% PEG400+0.5% Tween80+5% Propylene glycol: 30mg/kg
Synonyms
other peoduct :References PubMed ID::http://www.ncbi.nlm.nih.gov/pubmed/19395757
In Vitro |
In vitro activity: Dexamethasone results in decrease in transmonolayer paracellular permeability mainly to sucrose, fluorescein and dextrans of up to 20 KDa in an immortalised rat brain endothelial cell line (GPNT). Dexamethasone results in filamentous actin and the cytoskeleton associated protein cortactin being highly concentrated in the regions of cell-cell contact with few F-actin stress fibres visible within the cytoplasm in cultured rat brain endothelial cells, an observation consistent with a more differentiated barrier phenotype induced by dexamethasone. Dexamethasone treatment has been shown to strongly stimulate the level of the Id-1 protein, which is a serum-inducible helix-loop-helix transcriptional repressor, involved in cell differentiation, and this effect was shown to be associated with reorganisation of ZO-1 to the cell periphery in Con8 mammary epithelial tumor cells. Dexamethasone prevents cytokine-induced enhanced expression of MMP-9 and alterations in the expression of ZO-1 in untreated GPNT monolayers. Dexamethasone depletes both basal and TNF-alpha-stimulated GSH levels by down-regulating the gamma-GCS-heavy subunit transcription via a mechanism involving AP-1 (c-Jun) in alveolar epithelial cells. Dexamethasone decreases both basal and stimulated GSH levels (TNF-α-treated) in alveolar epithelial cells (A549), without any change in GSSG. Kinase Assay: Cell Assay: |
---|---|
In Vivo | Dexamethasone is administered i.m. to pregnant ewes, leads to the following results (1) blood pressure is unchanged; (2) as previously reported in the fetus, sensitivity to endothelin-1 (ET) is increased; (3) acetylcholine-induced relaxation is increased; (4) L-NAME suppressible vasodilatory response to ET is abolished; (5) there is no change in endothelium-independent vasodilatation; and (6) there is no change in eNOS RNA and protein levels, when compared to saline treated controls. |
Animal model | |
Formulation & Dosage | |
References | Neurosci Lett. 2003 Jun 26;344(2):112-6; J Physiol. 2003 Feb 15;547(Pt 1):61-6. |
Author: Sodium channel
product name Dexamethasone (DHAP)
Description: Dexamethasone (also known as DHAP) is a potent synthetic member of the glucocorticoid class of steroid drugs, and an interleukin receptor modulator that has anti-inflammatory and immunosuppressant effects. Dexamethasone has anti-inflammatory and immunosuppressant effects. It is 25-fold more potent than cortisol in its glucocorticoid effect, while having minimal mineralocorticoid effect. Dexamethasone is used for the treatment of many conditions including: rheumatologic problems, a number of skin diseases such as erythema multiforme, severe allergies, asthma etc.
References: Neurosci Lett. 2003 Jun 26;344(2):112-6; J Physiol. 2003 Feb 15;547(Pt 1):61-6.
392.46
Formula
C22H29FO5
CAS No.
50-02-2
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 79 mg/mL (201.3 mM)
Water: <1 mg/mL
Ethanol: 6 mg/mL (15.3 mM)
Solubility (In vivo)
30% PEG400+0.5% Tween80+5% Propylene glycol: 30mg/kg
Synonyms
other peoduct :References PubMed ID::http://www.ncbi.nlm.nih.gov/pubmed/19395757
In Vitro |
In vitro activity: Dexamethasone results in decrease in transmonolayer paracellular permeability mainly to sucrose, fluorescein and dextrans of up to 20 KDa in an immortalised rat brain endothelial cell line (GPNT). Dexamethasone results in filamentous actin and the cytoskeleton associated protein cortactin being highly concentrated in the regions of cell-cell contact with few F-actin stress fibres visible within the cytoplasm in cultured rat brain endothelial cells, an observation consistent with a more differentiated barrier phenotype induced by dexamethasone. Dexamethasone treatment has been shown to strongly stimulate the level of the Id-1 protein, which is a serum-inducible helix-loop-helix transcriptional repressor, involved in cell differentiation, and this effect was shown to be associated with reorganisation of ZO-1 to the cell periphery in Con8 mammary epithelial tumor cells. Dexamethasone prevents cytokine-induced enhanced expression of MMP-9 and alterations in the expression of ZO-1 in untreated GPNT monolayers. Dexamethasone depletes both basal and TNF-alpha-stimulated GSH levels by down-regulating the gamma-GCS-heavy subunit transcription via a mechanism involving AP-1 (c-Jun) in alveolar epithelial cells. Dexamethasone decreases both basal and stimulated GSH levels (TNF-α-treated) in alveolar epithelial cells (A549), without any change in GSSG. Kinase Assay: Cell Assay: |
---|---|
In Vivo | Dexamethasone is administered i.m. to pregnant ewes, leads to the following results (1) blood pressure is unchanged; (2) as previously reported in the fetus, sensitivity to endothelin-1 (ET) is increased; (3) acetylcholine-induced relaxation is increased; (4) L-NAME suppressible vasodilatory response to ET is abolished; (5) there is no change in endothelium-independent vasodilatation; and (6) there is no change in eNOS RNA and protein levels, when compared to saline treated controls. |
Animal model | |
Formulation & Dosage | |
References | Neurosci Lett. 2003 Jun 26;344(2):112-6; J Physiol. 2003 Feb 15;547(Pt 1):61-6. |