Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (5): 463-473.doi: 10.4103/1673-5374.130060

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Apolipoprotein E mimetic peptide protects against diffuse brain injury

Yaning Zhao 1, Jianmin Li 2, Qiqun Tang 1, Junling Gao 1, Changxiang Chen 1, Liwei Jing 1, Pan Zhang 1, Shuxing Li 1   

  1. 1 College of Rehabilitation, Hebei United University, Tangshan, Hebei Province, China
    2 Affiliated Hospital of Hebei United University, Tangshan, Hebei Province, China
  • Received:2013-11-25 Online:2014-03-12 Published:2014-03-12
  • Contact: Yaning Zhao, College of Rehabilitation, Hebei United University, Tangshan 063000, Hebei Province, China, zyning789@126.com.
  • Supported by:

    This study was supported by Scientific Research and Development Plan of Hebei Province, No. 20276102D; Key Project of Scientific Research in Universities of Hebei Province in China, No. ZD2010106.

Abstract:

Apolipoprotein E plays a crucial role in inhibiting chronic neurodegenerative processes. However, its impact on neurological function following diffuse brain injury is still unclear. This study was designed to evaluate the therapeutic effects and mechanisms of action of apolipoprotein E mimetic peptide on diffuse brain injury. Apolipoprotein E mimetic peptide was administered into the caudal vein of rats with diffuse brain injury  before and after injury. We found that apolipoprotein E mimetic peptide significantly decreased the number of apoptotic neurons, reduced extracellular signal-regulated kinase1/2 phosphorylation, down-regulated Bax and cytochrome c expression, decreased malondialdehyde content, and increased superoxide dismutase activity in a dose-dependent manner. These experimental findings demonstrate that apolipoprotein E mimetic peptide improves learning and memory function and protects against diffuse brain injury-induced apoptosis by inhibiting the extracellular signal-regulated kinase1/2-Bax mitochondrial apoptotic pathway.

Key words: nerve regeneration, brain injury, apolipoprotein E, diffuse brain injury, learning and memory, extracellular signal-regulated kinase, Bax, mitochondria, reactive oxygen species, apoptosis, Scientific Research and Development Plan of Hebei Province in China, neural regeneration