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Interleukin-1 receptor antagonist inhibits neuronal damage caused by fluid percussion injury in the rat.
Toulmond S, Rothwell NJ
Brain Res. 1995;671( 2):261-6.
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Abstract
Increased expression of the cytokine interleukin-1 (IL-1) has been observed in rodent and human brain after injury, and IL-1 has been implicated in ischaemic and excitotoxic brain damage in the rat. These data suggest that neurodegeneration caused by brain injury may be mediated by local IL-1 production and action. This hypothesis was tested by studying the effects of central injection of recombinant human interleukin-1 receptor antagonist (rhIL-1ra) on brain damage (assessed histologically, H and E stain) induced by fluid percussion trauma in the rat. Injection of rhIL-1ra (10 micrograms, i.c.v.) 15 min and 2, 4, 6, 8, 24 and 48 h after injury significantly reduced, by 44%, the extent of damage measured 3 days later. Similar protection was observed in animals killed 7 days after injury. Delayed administration of rhIL-1ra (4, 6, 8, 24 and 48 h) after injury also significantly reduced (by 28%) neuronal damage. These data indicate that endogenous IL-1 mediates damage caused by traumatic brain injury and that rhIL-1ra offers significant protection even when treatment is delayed.
Keyword(s)
Animals; Injections, Intraventricular; Male; Rats; Rats, Sprague-Dawley; Support, Non-U.S. Gov't; administration & dosage: Interleukin-1; administration & dosage: Recombinant Proteins; antagonists & inhibitors: Receptors, Interleukin-1; drug effects: Nerve Degeneration; drug effects: Neurons; pathology: Brain Injuries; pathology: Cerebral Cortex