Neural Regeneration Research

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Neuroprotective effect of rapamycin on spinal cord injury via activation of theWnt/β-catenin signaling pathway

Kai Gao 1, Yan-song Wang 1, Ya-jiang Yuan 1, Zhang-hui Wan 1, Tian-chen Yao 1, Hai-hong Li 1, Pei-fu Tang 2, Xi-fan Mei 1   

  1. 1 Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China
    2 Department of Orthopedics, General Hospital of Chinese PLA, Beijing, China
  • Online:2015-01-01 Published:2015-01-01
  • Contact: Xi-fan Mei, Ph.D.,meixifan1971@163.com. Pei-fu Tang, Ph.D., pftang301@163.com.
  • Supported by:

    This work was supported by grants from the National Natural Science Foundation of China, No. 81171799, 81471854 and a Special Financial Grant from the China Postdoctoral Science Foundation, No. 2013T60948.

Abstract:

The Wnt/β-catenin signaling pathway plays a crucial role in neural development, axonal guidance,neuropathic pain remission and neuronal survival. In this study, we initially examined the effect of rapamycin on the Wnt/β-catenin signaling pathway after spinal cord injury, by intraperitoneally injecting spinal cordinjured rats with rapamycinover 2 days. Western blot analysis and immunofluorescence staining were used to detect the expression levels of β-catenin protein, ca spase-3 protein and brain-derived neurotrophic factor protein,components of theWnt/β-catenin signaling pathway.Rapamycin increased the levels of β-catenin and brain-derived neurotrophic factor in the injured spinal cord, improved the pathological morphology at the injury site, reduced the loss of motor neurons, and promoted motor functional recovery in rats after spinal cord injury.Our experimental findings suggest that the neuroprotectiveeffect of rapamycin intervention is mediated through activation of the Wnt/β-catenin signaling pathway after spinal cord injury.

Key words: nerve regeneration, spinal cord injury, rapamycin, Wnt/β-catenin signaling pathway, apoptosis, caspase-3, brain-derived neurotrophic factor, neuroprotection, loss of neurons, NSFC grants, neural regeneration