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
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ISSN1673-5374
1876-7958
DOI10.4103/1673-5374.217335

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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.
AbstractList 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.
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.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.
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.
Audience Academic
Author Zhou, Zhi-qing
Wen, Zhi-li
Chen, Qi-wen
Huang, Zheng-gang
Li, Yong-liang
Ao, Zhen-bo
Yan, Xiao-hua
Xiao, Bing
AuthorAffiliation 5 Department of Neurosurgery, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
1 Department of Pediatrics, the Second People's Hospital of Huaihua City, Huaihua, Hunan Province, China
4 Department of Pediatrics, the First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
2 Department of Oncology, the Second People's Hospital of Huaihua City, Huaihua, Hunan Province, China
3 Department of Gastroenterology, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
AuthorAffiliation_xml – name: 5 Department of Neurosurgery, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
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– name: 3 Department of Gastroenterology, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
– name: 4 Department of Pediatrics, the First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
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Issue 10
Keywords 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
Language English
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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.
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Snippet Baicalin is a flavonoid compound extracted from Scutellaria baicalensis root. Recent evidence indicates that baicalin is neuroprotective in models of ischemic...
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StartPage 1625
SubjectTerms 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
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Title Baicalin protects neonatal rat brains against hypoxic-ischemic injury by upregulating glutamate transporter 1 via the phosphoinositide 3-kinase/protein kinase B signaling pathway
URI https://www.ncbi.nlm.nih.gov/pubmed/29171427
https://www.proquest.com/docview/2382693671
https://www.proquest.com/docview/1968444594
https://pubmed.ncbi.nlm.nih.gov/PMC5696843
https://doaj.org/article/7d0e2062cdab4ea48f9f6daa9f1a6ef7
Volume 12
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