Experimental brain injury induces expression of interleukin-1β mRNA in the rat brain

Cytokines have been shown to be induced following a variety of central nervous system (CNS) insults, and may play a role in the pathophysiological sequelae of CNS injury. In the present study, we characterized the regional expression of interleukin-1β (IL-1β) mRNA in specific brain regions following experimental lateral fluid-percussion traumatic brain injury (TBI) in rats. Adult Sprague-Dawley rats (n = 42) were anesthetized with sodium pentobarbital (60 mg/kg, i.p.) and subjected to lateral fluid-percussion brain injury of moderate severity (2.4 atm.) centered over the left parietal cortex, or ‘sham’ treatment (anesthesia and surgery without injury). Animals were sacrificed at 1, 6 and 24 h post injury, brains were removed, and tissue samples of left (injured) parietal cortex (LC), corresponding area in the contralateral right cortex (RC), cortex adjacent to injured parietal cortex (LA), corresponding adjacent area in the right cortex (RA), left hippocampus (LH) and right hippocampus (RH) were prepared. Total RNA was isolated and Northern blot hybridization was performed and the quantity of brain tissue IL-lβ mRNA is presented as percent relative radioactivity of IL-1β positive macrophage RNA which was loaded on same gel. At 1 h following brain injury, a marked and significant increase in expression of IL-113 mRNA was observed in LC (20.0 ± 0.7% of positive control, n = 6, P < 0.05 compared with sham animal), LH (24.5 ± 0.9%, p < 0.05) and LA (21.5 ± 3.1%, P < 0.05) in the injured hemisphere, which remained elevated up to 6 h post injury in the LC (4.0 ± 0.4%, n = 6, P < 0.05) and LH (5.0 ± 1.3%, P < 0.05). In sham or naive animals, no expression of IL-1β mRNA was observed in any of the respective brain areas. These results indicate that following TBI, the temporal expression of IL-113 mRNA is regionally stimulated in specific brain regions. these regional changes in cytokines, such as IL-1β may play a role in the post-traumatic pathologic or regenerative sequelae of brain injury.