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Corticosteroids mainly exert their anti-inflammatory effects by inhibiting the enzyme phospholipase A2. This inhibition plays a crucial role in modulating the inflammatory response because phospholipase A2 is responsible for the hydrolysis of membrane phospholipids, leading to the release of arachidonic acid. Arachidonic acid is a precursor for various pro-inflammatory mediators, including prostaglandins and leukotrienes, which are involved in inflammation processes. By preventing the release of arachidonic acid, corticosteroids effectively reduce the synthesis of these mediators, thus alleviating inflammation.

The other enzymes listed do not directly relate to the primary action of corticosteroids in the context of inflammation. HMG-CoA reductase is primarily involved in cholesterol synthesis, sphingomyelinase plays a role in sphingolipid metabolism, and β-glucocerebrosidase is implicated in the breakdown of glucocerebrosides. None of these enzymes contribute to the modulation of the inflammatory response in the same direct way that phospholipase A2 does.