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Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2),  the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.
Radiculopathy occurs when something irritates a spinal nerve—say a “slipped disc” causing a pinched nerve. This is also called sciatica . There are resident stem and other cells in the local tissues everywhere in our body. Many live around blood vessels. These are obviously also present in the disc and nerves in the epidural space and they usually play an important role in suppressing inflammation and repairing damage. We know, based on a copious in vitro (lab) data, that the high-dose steroids used in epidural injections can kill these cells. So the progression of the series of epidural steroid injections looks a little something like this: