title: Neuroprotective effects of infliximab in experimental spinal cord injury.
abstract: BACKGROUND
  The aim of the study is to assess the effects of infliximab, a TNF-alpha receptor blocker, in a spinal cord clip compression injury model.
  
  
  METHODS
  Clip compression injury model was used for producing spinal cord injury on 32 adult, male Wistar rats (Gazi University Animal Research Laboratory, Ankara, Turkey). After exposing the vertebral column between T7 and T10, total laminectomy was performed with the assistance of a high-speed drill and a surgical microscope. The dura was left intact. Spinal cord injury was performed on all rats with application of a 70-g closing force aneurysm clip for 1 minute. The rats were randomly allocated into 4 groups. Control group received no further therapy, whereas the other 3 groups received methylprednisolone (30 mg/kg intraperitoneal), infliximab (5 mg/kg subcutaneous), and a mixture of these 2 agents. All rats were killed 72 hours later, and the level of lipid peroxides in traumatized spinal cord tissue were measured as thiobarbituric acid-reactive material and determined using the method of Mihara and Uchiyama (Determination of malonaldehyde precursor in tissue by thiobarbituric acid test. Anal Biochem 1978;86(1):271-8).
  
  
  RESULTS
  Treatment with infliximab and methylprednisolone decreased MDA levels in rats with spinal cord injury with a statistically significant difference. In addition, combined therapy achieved a more profound decrease in tissue MDA levels, which was also statistically significant.
  
  
  CONCLUSIONS
  Infliximab is found as effective as methylprednisolone on spinal cord clip compression injury. Moreover, the combination of these 2 agents demonstrated higher efficacy suggesting a synergistic effect between these 2 agents. However, further studies regarding functional and behavioral analyses as well as biochemical markers are required.
authors.affiliation: Department of Neurosurgery, Gazi University Faculty of Medicine, 06500 Ankara, Turkey.
authors.forename: Gökhan
authors.initials: G
authors.lastname: Kurt
authors.forename: Ertan
authors.initials: E
authors.lastname: Ergün
authors.forename: Berker
authors.initials: B
authors.lastname: Cemil
authors.forename: Alp Ozgün
authors.initials: AO
authors.lastname: Börcek
authors.forename: Pelin
authors.initials: P
authors.lastname: Börcek
authors.forename: Ozlem
authors.initials: O
authors.lastname: Gülbahar
authors.forename: Necdet
authors.initials: N
authors.lastname: Ceviker
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D015415:Biomarkers / Q000378:metabolism; D004195:Disease Models, Animal; D000069285:Infliximab; D007274:Injections, Intraperitoneal; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008775:Methylprednisolone / Q000494:pharmacology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000187:drug effects; D013117:Spinal Cord Compression / Q000188:drug therapy* / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D015415:Biomarkers; D018696:Neuroprotective Agents; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D000069285:Infliximab; D008775:Methylprednisolone