Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/196863
Type: Artigo de periódico
Title: Bax And Bcl-2 Expression And Tunel Labeling In Lumbar Enlargement Of Neonatal Rats After Sciatic Axotomy And Melatonin Treatment.
Author: Rogério, Fábio
Jordão, Hamilton
Vieira, André Schwambach
Maria, Carla Cristina Judice
Santos de Rezende, Alexandre César
Pereira, Gonçalo Amarante Guimarães
Langone, Francesco
Abstract: Peripheral axotomy in neonatal rats induces neuronal death. We studied the anti-apoptotic protein Bcl-2 and cell death promoter Bax in spinal cord of neonatal rats after sciatic transection and treatment with melatonin, a neuroprotective substance. Pups were unilaterally axotomized at P2 and received melatonin (1 mg/kg; sc) or vehicle 1 h prior to lesion, immediately after, at 1 h, 2 h and then once daily. Rats were sacrificed at 3 h, 6 h, 24 h, 72 h and 5 days postaxotomy. Intact animals were used as controls. Lumbar enlargement was processed for Nissl staining, immunohistochemistry and RT-PCR for Bax or Bcl-2 and TUNEL reaction. Motoneurons (MN) of lesioned (L) and normal (N) sides were counted, and MN survival ratio (MSR=L/N) was calculated. Bax and Bcl-2 showed cytoplasmic immunoreactivity (IR). Bax IR was noticeable in small cells but less evident in MN. In unlesioned pups, some Bax-positive small cells (B+) and TUNEL-positive nuclei (T+) were mainly seen in the dorsal horn. In lesioned animals given vehicle, Bax mRNA levels and numbers of B+ and T+ were increased in comparison with intact controls at 24 h postaxotomy. The basal IR for Bax in MN was not changed by axotomy. Bcl-2 IR was noted in all cells and, like Bcl-2 mRNA, was unaltered after lesion. Melatonin reduced MN loss at 24 h, 72 h and 5 days and T+ at 24 h after lesion but did not interfere with Bax or Bcl-2 expression. These results suggest that (1) sciatic transection at P2 increases Bax mRNA and the amount of B+ and T+ in the lumbar enlargement, (2) Bax IR in immature MN is not altered by axotomy and (3) melatonin protects MN and dorsal horn cells through a mechanism independent of Bax and Bcl-2.
Subject: Analysis Of Variance
Animals
Animals, Newborn
Antioxidants
Axotomy
Cell Count
Disease Models, Animal
Gene Expression
Gene Expression Regulation, Developmental
In Situ Nick-end Labeling
Lumbosacral Region
Melatonin
Neurons
Proto-oncogene Proteins C-bcl-2
Rna, Messenger
Rats
Reverse Transcriptase Polymerase Chain Reaction
Sciatic Neuropathy
Spinal Cord
Time Factors
Bcl-2-associated X Protein
Citation: Brain Research. v. 1112, n. 1, p. 80-90, 2006-Sep.
Rights: fechado
Identifier DOI: 10.1016/j.brainres.2006.07.021
Address: http://www.ncbi.nlm.nih.gov/pubmed/16890920
Date Issue: 2006
Appears in Collections:Unicamp - Artigos e Outros Documentos

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