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P92 Background and Purpose: Inhibiting interleukin-1  action with its receptor antagonist (IL-1ra) followingpermanent middle cerebral artery occlusion (MCA-O) reduces  the volume of brain infarction and improves neurological function in  Wistar rats. We varied the times of IL-1ra administration and tested if  IL-1ra treatment reduces the lesion produced bytransient MCA-O (tMCA-O).Methods: One MCA was transiently occluded  for 1hr in 49 adult male Wistar rats. These animals were grouped  according to time of starting IL-1ra treatment (100 mg/Kg, 3  times/day): A) before MCA occlusion; B) at time of reperfusion); C)  after 1hr of reperfusion; and D) controls, i.e., placebo given at time  of reperfusion. Neurological function and body weight were measured on  the day of tMCA-O and daily thereafter. After 7 days of reperfusion,  fixed brain sections were obtained and either stained with H&amp;E or  immunostained for NeuN, GFAP, and ED-I (neuronal, astroglial, and  microglial proteins, respectively). Cellular damage was assessed using  quantitative image analysis.Results: Body weight and  neurological function were not significantly different among groups  A-D. Most rats of groups A-D had small, focal areas of pannecrosis in  the striatum at 7 days, but selective neuronal necrosis was the  predominant change in the cortex. In the striatum, the area of focal  infarction was less in IL-1ra treated groups than in placebo group, but  the difference was not statistically significant because of the  variability (i.e., large SD). The frequency (mean  number/mm2 ) of surviving neurons in the cortex (showing  strong positive nuclear staining with NeuN) was significantly greater  (p &lt; 0.001) in the treated groups (A = 532 ± 32;  B = 556 ± 33; and C = 588 ± 31) than the  untreated group (D = 276 ± 14).Conclusion: The  neuroprotective effects derived from reopening the artery after 1 hr of  MCA-O were enhanced by administering IL-1ra even when treatment was  started 1hr after beginning reperfusion. The protection induced by  treatment with IL-1ra seems to be more effective in cortex than  striatum.

Delayed treatment with interleukin-1 receptor antagonist protects cortical neurons from injury after transient MCA occlusion