MONDAY, April 24 (HealthDay News) -- The free radical-generating family of enzymes known as phospholipase A2 (PLA2) play a key role in cell destruction that occurs after spinal cord injury and blocking their action may represent a novel repair strategy, according to a study in rats published in the April issue of the Annals of Neurology.
Nai-Kui Liu, M.D., of the University of Louisville School of Medicine in Kentucky, and colleagues studied 108 rats that received contusive spinal cord injury and 66 rats that received injections of (PLA2) or melittin, an activator of endogenous PLA2.
The researchers found that both PLA2 activity and cytosolic PLA2 expression increased after spinal cord injury, with cytosolic PLA2 expression localized mainly in neurons and oligodendrocytes. They also found PLA2 and melittin could induce spinal neuronal death in vitro, which was substantially reversed by mepacrine, a PLA2 inhibitor. When they injected PLA2 into the normal spinal cord, they found that it induced confined demyelination, which was significantly reversed by mepacrine. When they injected melittin, they found that it induced diffuse tissue necrosis.
"It is conceivable that PLA2 acts as a common pathway for multiple key mechanisms of secondary injury, making it an attractive therapeutic target to improve tissue protection and functional recovery," state the authors of an accompanying editorial.
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