Bax And Bcl-2 Expression And Tunel Labeling In Lumbar Enlargement Of Neonatal Rats After Sciatic Axotomy And Melatonin Treatment.

dc.creatorRogério, Fábio
dc.creatorJordão, Hamilton
dc.creatorVieira, André Schwambach
dc.creatorMaria, Carla Cristina Judice
dc.creatorSantos de Rezende, Alexandre César
dc.creatorPereira, Gonçalo Amarante Guimarães
dc.creatorLangone, Francesco
dc.date2006-Sep
dc.date2015-11-27T13:05:39Z
dc.date2015-11-27T13:05:39Z
dc.date.accessioned2018-03-29T01:03:10Z
dc.date.available2018-03-29T01:03:10Z
dc.identifierBrain Research. v. 1112, n. 1, p. 80-90, 2006-Sep.
dc.identifier0006-8993
dc.identifier10.1016/j.brainres.2006.07.021
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/16890920
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/196863
dc.identifier16890920
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1297096
dc.descriptionPeripheral 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.
dc.description1112
dc.description80-90
dc.languageeng
dc.relationBrain Research
dc.relationBrain Res.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAnalysis Of Variance
dc.subjectAnimals
dc.subjectAnimals, Newborn
dc.subjectAntioxidants
dc.subjectAxotomy
dc.subjectCell Count
dc.subjectDisease Models, Animal
dc.subjectGene Expression
dc.subjectGene Expression Regulation, Developmental
dc.subjectIn Situ Nick-end Labeling
dc.subjectLumbosacral Region
dc.subjectMelatonin
dc.subjectNeurons
dc.subjectProto-oncogene Proteins C-bcl-2
dc.subjectRna, Messenger
dc.subjectRats
dc.subjectReverse Transcriptase Polymerase Chain Reaction
dc.subjectSciatic Neuropathy
dc.subjectSpinal Cord
dc.subjectTime Factors
dc.subjectBcl-2-associated X Protein
dc.titleBax And Bcl-2 Expression And Tunel Labeling In Lumbar Enlargement Of Neonatal Rats After Sciatic Axotomy And Melatonin Treatment.
dc.typeArtículos de revistas


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