Methylprednisolone (formerly NSC-19987; U-7532; NSC19987) is a synthetic glucocorticoid receptor agonist approved for use in the treatment of arthritis and bronchial inflammation or acute bronchitis. It is also used in the treatment of acute periods and long-term management of autoimmune diseases, most notably systemic lupus erythematosus.
理化性质和储存条件
| Molecular Weight (MW) | 374.47 |
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| Formula | C22H30O5 |
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| CAS No. | 83-43-2(Methylprednisolone); |
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| Storage | -20℃ for 3 years in powder form |
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| -80℃ for 2 years in solvent |
| Solubility (In vitro) | DMSO: 75 mg/mL (200.3 mM) |
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| Water:<1 mg/mL |
| Ethanol: 2 mg/mL (5.3 mM) |
SMILES
| O=C1C=C[C@]2(C)[C@@]3([H])[C@@H](O)C[C@]4(C)[C@@](O)(C(CO)=O)CC[C@@]4([H])[C@]3([H])C[C@H](C)C2=C1
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| Synonyms | NSC-19987; U-7532; NSC 19987; U 7532; NSC19987; U7532; |
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实验参考方法
| 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. |
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| 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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| Animal model | Rats |
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| Formulation & Dosage | 30 mg/kg |
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| References | Clin Exp Immunol. 1996 Oct;106(1):91-6; J Neurosci. 2003 Aug 6;23(18):6993-7000. |
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