Methylprednisolone

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. ^[1]

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. ^[2] 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. ^[3] 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. ^[4]