Role of immunoglobulin in neuronal apoptosis in a neonatal rat model of hypoxic ischemic brain injury.

Abstract

The objective of the present study was to evaluate the neuroprotective effects of immunoglobulin (Ig) in a neonatal hypoxic ischemic (HI) rat model. Seven-day-old rat pups were randomly assigned to control, hypoxia and hypoxia + Ig groups. The rats in the hypoxia +Ig group were intraperitoneally administered 1 g/kg Ig once, immediately after hypoxia. Saline was administered to the rats in the hypoxia group at the same time point. Eight rats from each of the Ig + hypoxia and hypoxia groups were sacrificed by decapitation 4 and 24 h following the administration of Ig or saline. The rats of the control group were sacrificed at the 4 h time-point. Caspase-3 activity, as well as IL-1β, IL-6 and TNF-α mRNA expression levels, were studied in the left ischemic hemispheres. Induction of cerebral ischemia increased the TNF-α, IL-6 and IL-1β mRNA expression levels significantly at 4 and 24 h in the left ischemic hemispheres in the hypoxia group compared with those in the control group. The systemic administration of Ig following HI encephalopathy significantly reduced the TNF-α, IL-6 and IL-1β mRNA expression levels in the ischemic tissue in the Ig + hypoxia group compared with those in the hypoxia group. In the hypoxia group, caspase-3 activity in the left half of the brain was found to be significantly increased compared with that in the control group. Caspase-3 activity in the Ig + hypoxia group was significantly lower than that in the hypoxia group. The observations of the present study indicate that Ig administration may be an efficient treatment approach for reducing cerebral apoptosis associated with hypoxic ischemia.