Chinese Journal Of Clinical Anatomy ›› 2017, Vol. 35 ›› Issue (2): 166-171.doi: 10.13418/j.issn.1001-165x.2017.02.010

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Expression changes of pEGFR after decompression of compressed spinal cord injury in rats

GONG Rui1, SUN Shan-quan1, ZHONG Yuan1, ZHANG Wei1, ZHAO Qi1, MU Ke-jie2, XUE Jun2   

  1. 1.Institute of Neuroscience, Chongqing Medical University, Chongqing 400016, China; 2.Department of Neurosurgery,Bishan Hospital, First Affiliated Hospital,Chongqing Medical University, Chongqing 402762, China
  • Received:2016-09-02 Online:2017-03-25 Published:2017-04-27

Abstract:

Objective To investigate the changes of pEGFR, pAkt1 expression in rat after decompression of compressed spinal cord injury(CSCI), and its correlation with nerve structure and function change,providing experimental basis for the development of therapeutic strategies and the development of medication for the treatment of CSCI after decompression. Methods The CSCI model was established first with a self-made device, which then underwent spinal decompression. The motor functions were monitored by Basso, Beattie & Bresnahanlocomotor rating scale. The pathological changes in axonal myelinated fibers were estimated by luxol fast blue (LFB). Epidermal growth factor receptor (EGFR), and phosphorylated Akt1 (pAkt1) were detected by double-labeling immunofluorescence and western blotting assays. Results The motor functions and number of myelinated nerve fibers were increased along with time extending after decompression. The expression of EGFR and pAkt1 was also increased after decompression, which was consistent with the changes of motor functions and number of myelinated nerve fibers. Conclusion The structure and function of the injured nerve can be restored to a certain extent, and the expression of pEGFR is closely related to this phenomenon after decompression. It suggests that the activation of EGFR is involved in the endogenous repair of CSCI after decompression.

Key words: Compressed spinal cord injury, Neural myelin sheaths, Demyelination, EGFR, pAkt1