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Neuroprotective effects of human recombinant interleukin-1 receptor antagonist in focal cerebral ischaemia in the rat.
Loddick S, Rothwell NJ
J Cereb Blood Flow Metab. 1996;16( 5):932-40.
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Abstract
Recombinant human interleukin-1 receptor antagonist (rhIL-1ra) markedly protects against focal cerebral ischaemia in the rat, implicating endogenous IL-1 in the events leading to cerebral infarction. The present experiments investigated the effect of intracerebroventricular (i.c.v.) administration of IL-1 beta or rhIL-1ra on ischaemia damage and physiological parameters after permanent middle cerebral artery occlusion in the rat. IL-1 beta (5 ng. i.c.v.) markedly (92%) enhanced infarct volume and caused a significant rise in body temperature, but rhIL-1ra (10 micrograms, i.c.v.) significantly reduced infarct volume and did not significantly affect heart rate, blood pressure, or body temperature, rhIL-1ra administered 30 min before, or at the time of ischaemia significantly reduced infarct volume in cortex (55 and 60%, respectively) and striatum (52 and 41%, respectively). rhIL-1ra administered 30 min after ischaemia significantly reduced total and cortical infarct volume (26 and 29%, respectively), but did not significantly protect striatal tissue. The effects of rhIL-1ra were still evident in both cortex and striatum 7 days after ischaemia. These results support the role of IL-1 in ischaemic brain damage, revealing potent, sustained, neuroprotective effects of rhIL-1ra in the cortex and striatum, which cannot be attributed directly to changes in physiological parameters.
Keyword(s)
Animals; Blood Pressure; Heart Rate; Human; Injections, Intraventricular; Male; Rats; Rats, Sprague-Dawley; Support, Non-U.S. Gov't; administration & dosage: Sialoglycoproteins; antagonists & inhibitors: Receptors, Interleukin-1; drug therapy: Ischemic Attack, Transient; pathology: Cerebral Cortex; pathology: Corpus Striatum; pharmacology: Recombinant Proteins