Neuronal tumour necrosis factor-α and interleukin-1β expression in a porcine model of intracerebral haemorrhage: Modulation by U-74389G

• We examine TNF-α and IL-1β changes in neurons after haematoma induction.
• The number of TNF-α and IL-1β increases early after haematoma induction.
• U-74389G suggests possible neuroprotective effect in our experiment.

Tumour necrosis factor α (TNF-α) and interleukin 1β (IL-1β) are important mediators of intracerebral haemorrhage (ICH) inflammatory response. Lazaroids, established antioxidants and neuroprotectants, have been studied in several brain pathologies. The present study was designed to investigate: a) TNF-α and IL-1β changes, in neurons and b) U-74389G effects, 4 and 24 h after haematoma induction in a porcine model of intracerebral haemorrhage.In twenty male landrace pigs (swines) aged 135–150 days old, autologous whole blood was injected around the right basal ganglia territory; in ten of the pigs the lazaroid compound U-74389G was administered. Brain TNF-α and IL-1β immunopositive neurons were determined by immunoarray techniques at 4 and 24 h timepoints.After the haematoma induction the number of TNF-α immunopositive neurons ipsilateral to the haematoma was significantly higher compared to the contralateral site at 4 h (p<0.0005), while U-74389G significantly reduced the number of TNF-α immunopositive neurons, ipsilateral to the haematoma, at 4 h (p=0.002); at 24 h, TNF-α immunopositive neurons were found significantly lower in the control group ipsilateral to the haematoma in comparison to 4 h timepoint(p<0.0005).The number of IL-1β immunopositive neurons at 4 h after the hematoma induction was significantly higher ipsilateral to the haematoma site (p<0.0005). U-74389G had no statistical significant effect.TNF-α and IL-1β, increase in neurons, 4 h after the haematoma induction, ipsilateral to the haematoma site. The administration of the antioxidant compound U-74389G, results in early (at 4 h) decrease of TNF-α immunopositive neurons but shows no statistical significant effect to IL-1β immunopossitive neurons.