title: Potential neuroprotective effect of Anakinra in spinal cord injury in an in vivo experimental animal model.
abstract: OBJECTIVE
  To evaluate the therapeutic effects of inhibiting interleukin-1 beta (IL-1 beta) in vivo using Anakinra in an experimental model of spinal cord injury (SCI).
  
  
  METHODS
  All experimental procedures were performed in the animal laboratory of Ankara Education and Research Hospital, Ankara, Turkey between August 2012 and May 2014. The SCI was induced by applying vascular clips to the dura via a 4-level T5-T8 laminectomy. Fifty-four rats were randomized into the following groups: controls (n = 18), SCI + saline (n = 18), and SCI + Anakinra (n = 18). Spinal cord samples were obtained from animals in both SCI groups at one, 6, and 24 hours after surgery (n = 6 for each time point). Spinal cord tissue and serum were extracted, and the levels of IL-1 beta, malondialdehyde, glutathione peroxidase, superoxide dismutase, and catalase were analyzed. Furthermore, histopathological evaluation of the tissues was performed.
  
  
  RESULTS
  The SCI in rats caused severe injury characterized by edema, neutrophil infiltration, and cytokine production followed by recruitment of other inflammatory cells, lipid peroxidation, and increased oxidative stress. After SCI, tissue and serum IL-1 beta levels were significantly increased, but were significantly decreased by Anakinra administration. Following trauma, glutathione peroxidase, superoxide dismutase, and catalase levels were decreased; however, Anakinra increased the activity of these antioxidant enzymes. Malondialdehyde levels were increased after trauma, but were unaffected by Anakinra. Histopathological analysis showed that Anakinra effectively protected the spinal cord tissue from injury.
  
  
  CONCLUSIONS
  Treatment with Anakinra reduces inflammation and other tissue injury events associated with SCI.
authors: Department of Neurosurgery, Oncology Training and Research Hospital, Demetevler, Ankara, Turkey. E-mail: aehasturk@yahoo.com.
authors: Askin E
authors: AE
authors: Hasturk
authors: Erdal R
authors: ER
authors: Yilmaz
authors: Erhan
authors: E
authors: Turkoglu
authors: Murat
authors: M
authors: Arikan
authors: Guray
authors: G
authors: Togral
authors: Nazli
authors: N
authors: Hayirli
authors: Berrin I
authors: BI
authors: Erguder
authors: Oya
authors: O
authors: Evirgen
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D023381:Endpoint Determination; D005979:Glutathione Peroxidase / Q000378:metabolism; D053590:Interleukin 1 Receptor Antagonist Protein / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000096:biosynthesis; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000188:drug therapy*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta; D018696:Neuroprotective Agents; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase