DL-2-amino-3-phosphonopropionic acid protects primary neurons from oxygen-glucose deprivation induced injury

Authors

  • Di Cui Department of Robot and Neuro-Rehabilitation, Ningbo Institute of Industrial Technology, Chinese Academy of Sciences, Ningbo, China; Department of Computer Science, Ningbo University of Technology, Ningbo, China
  • Jun Xu Department of Neurology, Yinzhou Second Hospital of Ningbo, Ningbo, China
  • Quanyi Xu Department of Pharmacy, Zhejiang Pharmaceutical College, Ningbo, China
  • Guokun Zuo Department of Robot and Neuro-Rehabilitation, Ningbo Institute of Industrial Technology, Chinese Academy of Sciences, Ningbo, China

DOI:

https://doi.org/10.17305/bjbms.2016.1553

Keywords:

DL-2-amino-3-phosphonopropionic acid, cerebral infarction, oxygen-glucose deprivation, neuron viability, apoptosis

Abstract

Cerebral infarction is a type of ischemic stroke and is one of the main causes of irreversible brain damage. Although multiple neuroprotective agents have been investigated recently, the potential of DL-2-amino-3-phosphonopropionic acid (DL-AP3) in treating oxygen-glucose deprivation (OGD)-induced neuronal injury, has not been clarified yet. This study was aimed to explore the role of DL-AP3 in primary neuronal cell cultures. Primary neurons were divided into four groups: (1) a control group that was not treated; (2) DL-AP3 group treated with 10 μM of DL-AP3; (3) OGD group, in which neurons were cultured under OGD conditions; and (4) OGD + DL-AP3 group, in which OGD model was first established and then the cells were treated with 10 μM of DL-AP3. Neuronal viability and apoptosis were measured using Cell Counting Kit-8 and flow cytometry. Expressions of phospho-Akt1 (p-Akt1) and cytochrome c were detected using Western blot. The results showed that DL-AP3 did not affect neuronal viability and apoptosis in DL-AP3 group, nor it changed p-Akt1 and cytochrome c expression (p > 0.05). In OGD + DL-AP3 group, DL-AP3 significantly attenuated the inhibitory effects of OGD on neuronal viability (p < 0.001), and reduced OGD induced apoptosis (p < 0.01). Additionally, the down-regulation of p-Akt1 and up-regulation of cytochrome c, induced by OGD, were recovered to some extent after DL-AP3 treatment (p < 0.05 or p < 0.001). Overall, DL-AP3 could protect primary neurons from OGD-induced injury by affecting the viability and apoptosis of neurons, and by regulating the expressions of p-Akt1 and cytochrome c.

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Author Biographies

  • Di Cui, Department of Robot and Neuro-Rehabilitation, Ningbo Institute of Industrial Technology, Chinese Academy of Sciences, Ningbo, China; Department of Computer Science, Ningbo University of Technology, Ningbo, China

    Department of Robot and Neuro-Rehabilitation;

    Department of Computer Science

  • Jun Xu, Department of Neurology, Yinzhou Second Hospital of Ningbo, Ningbo, China
    Department of Neurology
  • Quanyi Xu, Department of Pharmacy, Zhejiang Pharmaceutical College, Ningbo, China
    Department of Pharmacy
  • Guokun Zuo, Department of Robot and Neuro-Rehabilitation, Ningbo Institute of Industrial Technology, Chinese Academy of Sciences, Ningbo, China
    Department of Robot and Neuro-Rehabilitation

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DL-2-amino-3-phosphonopropionic acid protects primary neurons from oxygen-glucose deprivation induced injury

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Published

21-02-2017

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1.
DL-2-amino-3-phosphonopropionic acid protects primary neurons from oxygen-glucose deprivation induced injury. Biomol Biomed [Internet]. 2017 Feb. 21 [cited 2024 Apr. 20];17(1):12-6. Available from: https://www.bjbms.org/ojs/index.php/bjbms/article/view/1553