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

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...

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Published inNeural regeneration research Vol. 12; no. 10; pp. 1625 - 1631
Main Authors Zhou, Zhi-qing, Li, Yong-liang, Ao, Zhen-bo, Wen, Zhi-li, Chen, Qi-wen, Huang, Zheng-gang, Xiao, Bing, Yan, Xiao-hua
Format Journal Article
LanguageEnglish
Published India Medknow Publications and Media Pvt. Ltd 01.10.2017
Medknow Publications & Media Pvt. Ltd
Medknow Publications & Media Pvt Ltd
Wolters Kluwer Medknow Publications
Subjects
Alzheimer's disease
Brain
Brain damage
Care and treatment
Carotid arteries
Composition
Drug dosages
Encephalopathy
Flavonoids
Health aspects
Hypoxia
Ischemia
Kinases
Medicinal plants
nerve regeneration; baicalin; hypoxia ischemia; PI3K/Akt signaling pathway; glutamate transporter 1; excitotoxicity; neonatal rats; apoptosis; neural regeneration
Neurotransmitter receptors
Proteins
Rodents
Skullcap
Beijing China
United States > US
China
Germany
glutamate transporter 1
nerve regeneration; baicalin; hypoxia ischemia; PI3K/Akt signaling pathway; glutamate transporter 1; excitotoxicity; neonatal rats; apoptosis; neural regeneration
neural regeneration
baicalin
apoptosis
nerve regeneration
hypoxia ischemia
neonatal rats
PI3K/Akt signaling pathway
excitotoxicity
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ISSN1673-5374
1876-7958
DOI10.4103/1673-5374.217335

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Summary: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.
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Author contributions: XHY was responsible for the design of the experiments. QWC was responsible for establishing the animal model. ZQZ and YLL were responsible for molecular biology experiment. BX was responsible for experimental operation in 2,3,5-triphenyltetrazolium chloride, Nissl staining and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. ZGH was responsible for data collection. ZLW was responsible for statistical analysis. ZQZ wrote the paper. All authors approved the final version of the paper.
ISSN:1673-5374
1876-7958
DOI:10.4103/1673-5374.217335