Effect of Ketosis in the Hypoxic Brain Induced Caspase-3 Activation in Newborn Piglet

Perinatal hypoxic-ischemic (HI) brain injury is a major cause of permanent neurological dysfunction in children. Despite recent advances in understanding the pathogenesis of neonatal HI brain injury, currently, there is no effective treatment. The present study was conducted to test the hypothesis that the hypoxia-induced activation of caspase-3 in the cerebral cortex of newborn piglets is blocked by ketogenic diet. We use the animal model of the cerebral cortex of newborn piglets after hypoxia (7%O2) for 1 hour to test the neuroprotective effect of ketogenic diet. In this animal model, hypoxia can stimulate the excitotoxin (glutamate) to enter the intrinsic or mitochondrial pathway, further leading to activation of caspases-3 and neuron apoptosis. However, ketogenic diet is a older antiepileptic food. It is a high fat, adequate protein, low carbohydrate diet. The possible mechanisms of ketogenic diet are not yet well defined. In previous animal study of bialteral middle cerebral artery occlusion model of cerebral ischemia in the rat, exogenous administration of β- hydroxybutyrate, causing ketosis, can reduce brain damage and improve neuronal function and then demonstrated that ketosis possesses neuroprotective properties. So we use the animal model of the cerebral cortex of newborn piglets after hypoxia (7%O2) for 1 hour to test the neuroprotective effect of ketosis by measurement of caspases-3 concentration.

Project ID:PC9808-0595
External Project ID:NSC98-2314-B182-005