Corticosteroids exert anti-inflammatory effects primarily by which mechanism?

Corticosteroids exert anti-inflammatory effects primarily by which mechanism?

• A. Inhibiting Phospholipase A2
• B. Activating phospholipase C
• C. Stabilizing lysosomal membranes
• D. Blocking leukotriene synthesis

Answer: (A)

Corticosteroids work mainly by turning on the production of lipocortin (annexin I), which directly inhibits phospholipase A2. This enzyme normally releases arachidonic acid from membrane phospholipids, and arachidonic acid is the starting material for the inflammatory mediators prostaglandins, thromboxanes, and leukotrienes. So by blocking phospholipase A2, corticosteroids cut off the supply of arachidonic acid, leading to a broad suppression of these downstream inflammatory compounds and a reduction in inflammation. If phospholipase C were activated, it would boost signaling pathways that can promote inflammation, not suppress it, so that isn’t what corticosteroids do. Stabilizing lysosomal membranes can contribute to anti-inflammatory effects but is not the primary mechanism by which corticosteroids achieve their broad anti-inflammatory action. Blocking leukotriene synthesis directly would require targeting the lipoxygenase pathway, whereas corticosteroids mainly prevent the initial release of arachidonic acid, thus reducing all downstream products, including leukotrienes, prostaglandins, and thromboxanes.

Corticosteroids work mainly by turning on the production of lipocortin (annexin I), which directly inhibits phospholipase A2. This enzyme normally releases arachidonic acid from membrane phospholipids, and arachidonic acid is the starting material for the inflammatory mediators prostaglandins, thromboxanes, and leukotrienes. So by blocking phospholipase A2, corticosteroids cut off the supply of arachidonic acid, leading to a broad suppression of these downstream inflammatory compounds and a reduction in inflammation.

If phospholipase C were activated, it would boost signaling pathways that can promote inflammation, not suppress it, so that isn’t what corticosteroids do. Stabilizing lysosomal membranes can contribute to anti-inflammatory effects but is not the primary mechanism by which corticosteroids achieve their broad anti-inflammatory action. Blocking leukotriene synthesis directly would require targeting the lipoxygenase pathway, whereas corticosteroids mainly prevent the initial release of arachidonic acid, thus reducing all downstream products, including leukotrienes, prostaglandins, and thromboxanes.