title: The pathological changes in the spinal cord after dural tear with and without autologous fascia repair.
abstract: OBJECTIVE
  Dural tear is one of the common complications of spinal surgery leading to cerebrospinal fluid leakage followed by serial secondary symptoms. However, little is known about pathological changes of the spinal cord after dural tear. In the present study, we aimed to study the pathological changes in the spinal cord after dural tear with and without autologous fascia repair.
  
  
  METHODS
  Sixty Sprague-Dawley rats were used for dural tear and autologous fascia graft repair models. Three days and 1 week after surgery, the pathological changes in the spinal cord were analyzed by immunohistochemistry, Western blot, enzyme-linked immunosorbent assay and spinal somatosensory evoked potentials test.
  
  
  RESULTS
  Neuroinflammation was found in the parenchyma of the spinal cord characterized by gliosis, increased expression of inflammatory factors and infiltration of exogenesis immunocells in the rats without repair, which impaired the sensory conduction function of the spinal cord at the early stage of injury. Repairing with autologous fascia could attenuate neuroinflammation and help to maintain normal sensory conduction function of the spinal cord.
  
  
  CONCLUSIONS
  Dural tear could cause a series of inflammatory reactions in the spinal cord and further impair its sensory conduction function at the early stage of injury. Repairing with autologous fascia was a necessary and effective way to prevent the neuroinflammation and to maintain the normal function of the spinal cord.
authors.affiliation: Graduate School of Dalian Medical University, Dalian, 116044, Liaoning, China, songyi19800913@163.com.
authors.forename: Yi
authors.initials: Y
authors.lastname: Song
authors.forename: Shao
authors.initials: S
authors.lastname: Li
authors.forename: Bo
authors.initials: B
authors.lastname: Song
authors.forename: Yanli
authors.initials: Y
authors.lastname: Zhang
authors.forename: Wenting
authors.initials: W
authors.lastname: Gao
authors.forename: Ning
authors.initials: N
authors.lastname: Li
authors.forename: Kai
authors.initials: K
authors.lastname: Fan
authors.forename: Jianmei
authors.initials: J
authors.lastname: Ma
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D015153:Blotting, Western; D004388:Dura Mater / Q000293:injuries* / Q000601:surgery; D004797:Enzyme-Linked Immunosorbent Assay; D005205:Fascia / Q000637:transplantation*; D005260:Female; D005904:Glial Fibrillary Acidic Protein; D005911:Gliosis / Q000473:pathology; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology; D053583:Interleukin-1beta / Q000378:metabolism; D017628:Microglia / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology*; D014182:Transplantation, Autologous
chemical_list: D005904:Glial Fibrillary Acidic Protein; D053583:Interleukin-1beta; D009419:Nerve Tissue Proteins; C528900:glial fibrillary astrocytic protein, mouse; D052247:Nitric Oxide Synthase Type II