Changes of cervical dorsal root ganglia induced by compression injury and decompression procedure: a novel rat model of cervical radiculoneuropathy.
Our study aimed to establish a model of compression injury of cervical dorsal root ganglia (DRG) in the rat and to investigate the pathological changes following compression injury and decompression procedures. Thirty rats were divided into three groups: control group receiving sham surgery, compression group undergoing surgery to place a micro-silica gel on C6 DRG, and decompression group with subsequent decompression procedure. The samples harvested from the different groups were examined with light microscopy, ultrastructural analysis, and horseradish peroxidase (HRP) retrograde tracing techniques. Apoptosis of DRG neurons was demonstrated with TUNEL staining. Changes in PGE2 and PLA2 in DRG neurons were detected with enzyme-linked immunosorbent assay (ELISA). Local expression of vascular endothelial growth factor (VEGF) was monitored with immunohistochemistry. DRG neurons in the compression group became swollen with vacuolar changes in cytoplasm. Decompression procedure partially ameliorated the resultant compression pathology. Ultrastructural examination showed a large number of swollen vacuoles, demyelinated nerve root fibers, absence of Schwann cells, and proliferation in the surrounding connective tissues in the compression group. Compared to the control group, the compression group showed a significant decrease in the number of the HRP-labeled cells and a significant increase in levels of PGE2 and PLA2, in the expression of VEGF protein, and in the number of apoptotic DRG neurons. These findings demonstrate that compression results in local inflammation, followed by increased apoptosis and upregulation of VEGF. We conclude that such a model provides a tool to study the pathogenesis and treatment of cervical radiculoneuropathy.
Tang
Zhan-Ying
ZY
Institute of Spine, Shanghai University of Traditional Chinese Medicine, Shanghai, P. R. China.
Shu
Bing
B
Cui
Xue-Jun
XJ
Zhou
Chong-Jian
CJ
Shi
Qi
Q
Holz
Jonathan
J
Wang
Yong-Jun
YJ
D000818:Animals; D017209:Apoptosis; D019299:Decompression, Surgical; D015232:Dinoprostone / Q000378:metabolism; D004195:Disease Models, Animal; D005727:Ganglia, Spinal / Q000293:injuries* / Q000473:pathology / Q000648:ultrastructure; D006735:Horseradish Peroxidase; D007150:Immunohistochemistry; D008297:Male; D046529:Microscopy, Electron, Transmission; D009408:Nerve Compression Syndromes / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D054467:Phospholipases A2 / Q000378:metabolism; D011843:Radiculopathy / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013194:Staining and Labeling; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D006735:Horseradish Peroxidase; D054467:Phospholipases A2; D015232:Dinoprostone