Pharmacological Effects of Glucocorticoids

Inhibiting phospholipase A2 activity, thereby decreasing the synthesis of PGE2 and of the potent chemotactic substance leukotriene B4 

Stabilizing membranes of the lysosomes and secretory granules, thereby inhibiting the release of their contents, and 

Acting directly on the capillary endothelium to render it less permeable. 

This endothelial effect and the permissive effect of glucocorticoids on catecholamine-induced vasoconstriction inhibit edema and swelling. Use of glucocorticoids to reduce inflammation due to bacterial infection should not be undertaken without concurrent use of antibiotics. 

It has been suggested that the decline in DHEA and DHEAS production after adrenopause may be causally related to age-related health problems and that DHEA replacement may reduce the aging process. Evidence to date from animal and human studies that involved the administration of DHEA appears to support the idea that 

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Most of the established pharmacological effects of glucocorticoids are mediated by cytoplasmic glucocorticoid receptors. After binding to the receptor, the steroid-receptor complex binds to chromatin and stimulate the formation of mRNA. The mRNA stimulates the synthesis of enzymes which produce various pharmacological actions. 

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