Pharmacology: Methylprednisolone is a glucocorticoid prednisolone derivative which has the same effect and usage with its parent agents. It does not have sodium retention activity like other glucocorticoids. Methylprednisolone is an intermediate acting corticosteroid, classified as an adrenocorticoid, anti-inflammatory and immunosuppressant category.
Adrenocorticoid Effect: Like adrenocorticoids, Methylprednisolone diffuses across the membrane and concurrently with cytoplasmic receptor forms specific 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 to the effect of systemic adrenocorticoid. However, Methylprednisolone may suppress transcription of mRNA in some cells (e.g., lymphocytes).
Glucocorticoid Effects: Anti-inflammatory (steroidal): Glucocorticoid decrease and prevent tissue responses to inflammatory processes, thereby reducing the inflammation symptoms without affecting underlying cause.
Glucocorticoids inhibit accumulation of inflammatory cells, including macrophages and leucocytes at the inflammation site. Methylprednisolone also inhibits phagocytosis, lysosomal enzyme release, synthesis or release of several chemical mediator of inflammation. Although the exact mechanism has not completely been understood, the possible effect is blocking macrophage inhibitory factor (MIF), inhibits macrophage localization, reduction or dilatation permeability of inflammed capillaries and reduction of leucocyte adherence in the capillary endothelium, inhibits oedema formation and leucocyte migration, and increase synthesis of lipomodulin (macrocortin), an inhibitor of phospholipase A2-mediator arachidonic acid release from phospholipid membrane and subsequent inhibition of the synthesis of arachidonic acid mediators derivative (prostaglandins, thromboxane and leucotrienes). Immunosuppressant actions may also influence anti-inflammatory effect.
Immunosuppressant: Mechanism of action of immunosuppressants have not been completely understood, but may involve prevention or suppression of cell-mediated (delayed hypersensitivity) immune reaction as well as more specific treatment that influence immune response. Glucocorticoids reduce thymus lymphocyte concentration (T-lymphocyte), monocyte and eosinophil. Methylprednisolone also decreases immunoglobulin binding to cell surface receptors and inhibits 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.
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