title: Neuroprotective effects of infliximab in experimental spinal cord ischemic injury.
abstract: Reactive oxygen species (ROS) have been implicated in the pathogenesis of spinal cord injury after both ischemia-reperfusion (I/R) and trauma. This experimental study was designed to investigate the potential effects of infliximab, an anti-tumor necrosis factor-α agent, on I/R injury of the rabbit spinal cord. Eighteen New Zealand white rabbits were divided into three groups, each consisting of six rabbits: sham (no I/R), I/R, and infliximab (I/R + infliximab). Spinal cord ischemia was induced by applying an infrarenal aortic cross clamp for 30 minutes. At 48 hours after ischemia, animals were functionally evaluated using the Tarlov score. Changes in the spinal cord were observed by measuring tissue levels of malondialdehyde (MDA), glutathione (GSH), advanced oxidation protein products (AOPP), and superoxide dismutase (SOD) and by evaluating hematoxylin-eosin-stained sections. At 48 hours after ischemia, the Tarlov scores in the infliximab group were higher than those of the I/R group, MDA and AOPP levels in the I/R group were significantly higher than those in the sham and infliximab groups (p < 0.05), and SOD levels in the infliximab group were significantly higher than those in the I/R and sham groups (p < 0.05). The sham group had higher GSH levels than the infliximab group; however, the difference was not statistically significant (p > 0.05). Histological examination revealed that the infliximab group had significantly less vascular proliferation, edema, and neuron loss than the I/R group. These results indicate that infliximab may protect the spinal cord against injury in a rabbit I/R model.
authors.affiliation: Department of Neurosurgery, Gazi University, Faculty of Medicine, Beşevler, Ankara 06500, Turkey.
authors.forename: Cagatay
authors.initials: C
authors.lastname: Guven
authors.forename: Alp Ozgun
authors.initials: AO
authors.lastname: Borcek
authors.forename: Berker
authors.initials: B
authors.lastname: Cemil
authors.forename: Gokhan
authors.initials: G
authors.lastname: Kurt
authors.forename: Zuhal
authors.initials: Z
authors.lastname: Yildirim
authors.forename: Nese Lortlar
authors.initials: NL
authors.lastname: Ucankus
authors.forename: Nedret
authors.initials: N
authors.lastname: Kilic
authors.forename: Necdet
authors.initials: N
authors.lastname: Ceviker
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D000069285:Infliximab; D008315:Malondialdehyde / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D011817:Rabbits; D013119:Spinal Cord Injuries / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D020760:Spinal Cord Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D018696:Neuroprotective Agents; D008315:Malondialdehyde; D000069285:Infliximab; D013482:Superoxide Dismutase; D005978:Glutathione