Baicalin protects neonatal rat brains against hypoxic-ischemic injury by upregulating glutamate transporter 1 via the phosphoinositide 3-kinase/protein kinase B signaling pathway

Abstract

Baicalin is a flavonoid compound extracted from Scutellaria baicalensis root. Recent evidence indicates that baicalin is neuroprotective in models of ischemic stroke. Here, we investigate the neuroprotective effect of baicalin in a neonatal rat model of hypoxic-ischemic encephalopathy. Seven-day-old pups underwent left common carotid artery ligation followed by hypoxia (8% oxygen at 37°C) for 2 hours, before being injected with baicalin (120 mg/kg intraperitoneally) and examined 24 hours later. Baicalin effectively reduced cerebral infarct volume and neuronal loss, inhibited apoptosis, and upregulated the expression of p-Akt and glutamate transporter 1. Intracerebroventricular injection of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) inhibitor LY294002 30 minutes before injury blocked the effect of baicalin on p-Akt and glutamate transporter 1, and weakened the associated neuroprotective effect. Our findings provide the first evidence, to our knowledge that baicalin can protect neonatal rat brains against hypoxic-ischemic injury by upregulating glutamate transporter 1 via the PI3K/Akt signaling pathway.

Keywords

• nerve regeneration; baicalin; hypoxia ischemia; PI3K/Akt signaling pathway; glutamate transporter 1; excitotoxicity; neonatal rats; apoptosis; neural regeneration