Medixon Mechanism of Action

Pharmacology: Methylprednisolone is an intermediate-acting corticosteroid. It is a glucocorticoid prednisolone derivative which has the same activity and use to the main compound. It is classified as an adrenocorticoid with anti-inflammatory and immunosuppressant actions, and has no sodium retention like other glucocorticoids.
Adrenocorticoid: Like other adrenocorticoids, methylprednisolone diffuses across the membranes and concurrently with specific cytoplasmic receptor forming a complex. These complexes then enter the cell nucleus, bind to DNA and stimulate transcription of messenger RNA (mRNA) and subsequent protein synthesis of various enzymes thought to be responsible for the effect of systemic adrenocorticoids. However, methylprednisolone may suppress transcription of mRNA in some cells (eg, lymphocytes).
Glucocorticoid Effects: Anti-Inflammatory (Steroidal): Glucocorticoids decrease or prevent tissue responses to inflammatory process, thereby reducing the inflammation symptoms without affecting underlying cause. Glucocorticoids inhibit accumulation of inflammatory cells, including macrophages and leukocytes at the inflammation site. Methylprednisolone also inhibits phagocytosis, lysosomal enzyme release and synthesis or release of several chemical mediators of inflammation. Although the exact mechanism has not been completely known, the possible effect is blocking of macrophage inhibitory factor (MIF), inhibition of macrophage localization, reduction or dilatation of inflamed permeable capillaries and reduction of leukocyte adherence in the capillary endothelium, inhibition of edema formation and leukocyte migration, and increased synthesis of lipomodulin (macrocortin), an inhibitor of phospholipase A2-mediator arachidonic acid released from phospholipid membrane, and subsequent inhibition of the synthesis of arachidonic acid inflammatory mediators derivative (prostaglandins, thromboxane and leukotrienes). Immunosuppressant actions may also influence anti-inflammatory effect.
Immunosuppressant: Mechanism of action of immunosuppressant effect has not been completely known, but may involve the prevention or suppression of mediated-cell (delayed hypersensitivity), immune reaction as well as more specific treatment that influence immune response. Glucocorticoids reduce thymus lymphocyte concentration (T-lymphocyte), monocytes and eosinophils. Methylprednisolone also decreases immunoglobulin-binding to cell surface receptors and inhibit synthesis and/or release of interleukins, thereby decreasing T-lymphocyte blastogenesis and reducing expansion of primary immune response. Glucocorticoids may also decrease passage of immune complexes through basement membranes and decrease concentration of complement components and immunoglobulin.