Cortisone can decrease the signaling of eicosenoids derived from arachidonic acid by inhibiting:

Question

BlackTom AI · Accepted Answer

Let's parse the question step by step and lay out the options clearly before judging them.
Option 1: 'nerve transmission to the brain' — Corticosteroids like cortisone can affect many inflammatory and signaling pathways, but nerve transmission to the brain is not a primary target of corticosteroids through inhibition of arachidonate-derived eicosanoids. This choice misattributes the main anti-inflammatory mechanism to neural signaling processes rather than lipid mediator synthesis.
Option 2: 'arachidonic acid production by Phospholipase A2' — This statement aligns with the known mechanism by which glucocorticoids reduce the synthesis of eicosanoids. Cortisone and other glucocorticoids inhibit phospholipase A2 (via induction of annexin-1/annexin II in some contexts), thereby decreasing liberation of arachidonic acid from membrane phospholipids, which in turn reduces downstream production of prostaglandins and leukotrienes. This is a direct and well-established pathway affecting eicosanoid signaling.
Option 3: 'glucose oxidation in Glycolysis' — While glucocorticoids can influence metabolic processes, including gluconeogenesis and protein catabolism, their impact on glycolytic glucose oxidation is not the principal mechanism by which they diminish signaling from eicosanoids derived from arachidonic acid. This option targets a separate metabolic pathway unrelated to the immediate control of arachidonic acid–derived mediators.
In terms of conceptual accuracy, the core idea behind corticosteroid action here is the suppression of arachidonic acid release from membrane phospholipids, which reduces the substrate availability for the cyclooxygenase and lipoxygenase pathways that generate eicosanoids. The neural signaling option does not capture this lipid mediator–synthesis mechanism, and the glycolysis option addresses a different metabolic arena altogether.
Overall, option 2 directly reflects the pharmacologic effect of cortisone on the signaling cascade mediated by eicosanoids, while options 1 and 3 describe aspects that are not central to this mechanism and are therefore inaccurate in this specific context.

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