Abstract
Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe brain disease that often leads to death or irreversible sequelae. The aim of this study was to determine the effect of a naturally active drug (grape seed proanthocyanidin extract [GSPE]) on the expression of autophagic proteins in a mouse model of neonatal hypoxic-ischemic brain injury. In this study immunofluorescence staining and Western blotting were used to detect the expression of autophagy markers (LC3II and beclin1) in the brains of neonatal mice with hypoxic-ischemic brain injuries after GSPE administration. Our study showed that GSPE pre-treatment down-regulates LC3II and beclin-1 expression, thus GSPE may be a potential drug for the treatment of HIE.
Highlights
Hypoxic-ischemic encephalopathy (HIE) is a severe brain injury with various causes in the perinatal period
The results of our preliminary studies have demonstrated that Grape seed proanthocyanidin extract (GSPE) significantly improves cerebral infarction volume and neurobehavior in a murine model of HIE, and GSPE pre-treatment attenuates apoptosis through the bax/bcl2-cleaved caspase3 signaling pathway
On day 3 after HI injury, we observed a significant increase in the expression of LC3II and beclin1 proteins in the HI group
Summary
Hypoxic-ischemic encephalopathy (HIE) is a severe brain injury with various causes in the perinatal period. HIE is often accompanied by high mortality and disability rates [1, 2]. Neonatal asphyxia occurs in 2-4 of 10,000 full-term newborns, and 20%-50% die as a result of HIE during the neonatal period. The survivors often have serious sequelae, such as epilepsy, cerebral palsy, and mental retardation [3]. Children with HIE often undergo hypothermia therapy [4]. Hypothermia therapy has a good curative effect in patients with mild-to-moderate brain injury, but hypothermia therapy has little effect in patients with severe HIE brain injuries [5]. There is an urgent need to identify a targeted drug to treat HIE
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