title: [Injury markers in two models of cerebral ischemia].
abstract: BACKGROUND
  Spatio-temporal indicators of injury are essential for the study of neuropathological processes and for developing therapeutic approaches for stroke.
  
  
  OBJECTIVE
  This study sought to optimize the techniques of two cerebral ischemia models (focal and global) and to comparatively evaluate the progression of brain damage by analyzing markers of neurodegeneration.
  
  
  METHODS
  Wistar rats were subjected to temporary occlusion of the middle cerebral artery (t-MCAO) or four-vessel occlusion (4-VO), and surgical time, survival rate and neurological recovery were comparatively evaluated. Triphenyl tetrazolium was used to determine the distribution of the infarction, and Fluoro-Jade B was used as a marker of neurodegeneration. Astroglial immunoreactivity was assessed with an anti-glial fibrillary acidic protein (GFAP) antibody, and an anti-AT-8 antibody was used to detect hyperphosphorylated tau protein at 24, 48 and 72 hours post-ischemia.
  
  
  RESULTS
  The cerebral ischemia models employed (t-MCAO and 4-VO) required less surgical time and presented less of a death risk compared to those in previous studies. In the focal model, Fluoro-Jadepositive cells and reactive astrocytes were observed in the cerebral cortex and the hippocampus at 24 hours post-ischemia. In the global model, we observed Fluoro-Jade-positive cells at 24 hours, and a significant increase in the reactivity of GFAP was observed at 72 hours in the cortex and at 48 hours in the hippocampus. The immunoreactivity of hyperphosphorylated tau protein increased progressively, reaching a maximum at 72 hours post-ischemia in both models.
  
  
  CONCLUSIONS
  These results suggest that in the t-MCAO and 4-VO ischemia models, the expression of Fluoro-Jade and GFAP indicates early neurodegeneration at 24 hours post-insult. In contrast, the immunoreactivity of the hyperphosphorylated tau protein marker (AT-8) progressively increases until 72 hours post-insult, which suggests that the progression of excitotoxicity and alteration of enzymes involves the phosphorylation of cytoskeletal proteins.
authors.affiliation: Departamento de Salud Animal, Grupo Grupo de Investigación en Enfermedades Neurodegenerativas, Facultad de Medicina Veterinaria, Universidad del Tolima, Tolima, Ibagué, Colombia.
authors.forename: Angel Enrique
authors.initials: AE
authors.lastname: Céspedes
authors.affiliation: Fundación Valle del Lili, Cali, Colombia.
authors.forename: César Augusto
authors.initials: CA
authors.lastname: Arango
authors.affiliation: Área de Neurobiología Celular y Molecular, Grupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
authors.forename: Gloria Patricia
authors.initials: GP
authors.lastname: Cardona
mesh_terms: D000818:Animals; D015415:Biomarkers; D002545:Brain Ischemia / Q000175:diagnosis / Q000276:immunology; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D005452:Fluoresceins; D005904:Glial Fibrillary Acidic Protein; D010766:Phosphorylation; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D016875:tau Proteins / Q000378:metabolism
chemical_list: D015415:Biomarkers; D005452:Fluoresceins; D005904:Glial Fibrillary Acidic Protein; C435731:fluoro jade; D016875:tau Proteins