product name Methylprednisolone
Description: Methylprednisolone (also known as NSC-19987) is a synthetic glucocorticoid receptor agonist, used to achieve prompt suppression of inflammation. It is used in arthritis therapy and short-term treatment of bronchial inflammation or acute bronchitis due to various respiratory diseases. It is also used both in the treatment of acute periods and long-term management of autoimmune diseases, most notably systemic lupus erythematosus.
References: Clin Exp Immunol. 1996 Oct;106(1):91-6; J Neurosci. 2003 Aug 6;23(18):6993-7000.
374.47
Formula
C22H30O5
CAS No.
83-43-2
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 75 mg/mL (200.3 mM)
Water: <1 mg/mL
Ethanol: 2 mg/mL (5.3 mM)
Solubility (In vivo)
Synonyms
NSC-19987
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19422583
| In Vitro |
In vitro activity: Methylprednisolone (2-10 mg/kg) markedly inhibits TNF production but does not affect serum levels of IL-10, while a high methylprednisolone dose (50 mg/kg) increases LPS-induced IL-10 levels. Methylprednisolone(from 0.01 to 100 mg/mL) also increases the biosynthesis of IL-10 by LPS-activated mouse peritoneal macrophages. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Methylprednisolone decreases RGC survival in rats with electrophysiologically diagnosed optic neuritis. Methylprednisolone decreases RGC survival by a nongenomic, calcium-dependent mechanism. Methylprednisolone-induced enhancement of RGC degeneration depends on calcium influx through voltage-gated calcium channels. Methylprednisolone treatment leads to a significant decrease in the number of ED1-positive cells in both rostral and caudal stumps. Methylprednisolone treatment results in a significant reduction in tissue loss in both cord stumps at 2, 4 and 8 week post-injury. Methylprednisolone leads to a long-term reduction of ED1-positive cells and spinal tissue loss, reduced dieback of vestibulospinal fibres, and a transient sprouting of vestibulospinal fibres near the lesion at 1 and 2 weeks post-lesion. Methylprednisolone at a dose of 30 mg/kg which has been shown to be effective in improving functional outcomes in rat SCI models, suppresses TNF-α expression and NF-kB activation. Methylprednisolone inhibition of NF-kB function is likely mediated by the induction of IkB, which traps NF-kB in inactive cytoplasmic complexes. |
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| References | Clin Exp Immunol. 1996 Oct;106(1):91-6; J Neurosci. 2003 Aug 6;23(18):6993-7000. |
