Neural Regeneration Research ›› 2017, Vol. 12 ›› Issue (10): 1625-1631.doi: 10.4103/1673-5374.217335

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

Zhi-qing Zhou1, Yong-liang Li2, Zhen-bo Ao1, Zhi-li Wen3, Qi-wen Chen4, Zheng-gang Huang4, Bing Xiao5, Xiao-hua Yan4   

  1. 1 Department of Pediatrics, the Second People’s Hospital of Huaihua City, Huaihua, Hunan 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
    4 Department of Pediatrics, the First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
    5 Department of Neurosurgery, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China
  • Received:2017-09-04 Online:2017-10-15 Published:2017-10-15
  • Contact: Xiao-hua Yan, M.D.,yanxiaohua456@aliyun.com.
  • Supported by:

    This study was supported by the Chinese Medicine Research Foundation of Jiangxi Provincial Health Department of China, No.2013A040; the Science and Technology Program of Jiangxi Provincial Health Department of China, No. 20123023; and the Science and Technology Support Program of Jiangxi Province of China, No. 2009BSB11209.

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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.

Key words: nerve regeneration, baicalin, hypoxia ischemia, PI3K/Akt signaling pathway, glutamate transporter 1, excitotoxicity, neonatal rats, apoptosis, neural regeneration