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- Title
Erythropoietin can promote survival of cerebral cells by downregulating Bax gene after traumatic brain injury in rats.
- Authors
Liao, Z. B.; Jiang, G. Y.; Tang, Z. H.; Zhi, X. G.; Sun, X. C.; Tang, W. Y.; Wu1, M. J.
- Abstract
Background: Traumatic brain injury (TBI) is an important cause of adult mortality and morbidity. Erythropoietin (Epo) has been shown to promote the viability of cerebral cells by upregulating Bcl-2 gene; however, Epo may exert its antiapoptotic effect via the differential regulation of the expression of genes involved in the apoptotic process. Aim: The present study examined the neuroprotective effect of Epo as a survival factor through the regulation of the Bax. Materials and Methods: Wistar rats were randomly divided into three groups: Recombinant human EPO treated (rhEPO) TBI, vehicle-treated TBI, and sham-operated. Traumatic brain injury was induced by the Feeney free-falling model. Rats were killed 5, 12, 24, 72, 120, or 168 h after TBI. Regulation of Bcl-2 was detected by reverse transcription-polymerase chain reaction (RT-PCR), western blotting and immunofluorescence. Results: Bax mRNA and protein levels were lower in the rhEPO)-treated rat brains than in the vehicle-treated rat brains. Induction of Bax expression peaked at 24 h and remained stable for 72-120 h in vehicle-treated rat brains, whereas induction of Bax expression was only slightly elevated in rhEPO-treated rat brains. The number of TdT-mediated dUTP Nick-End Labeling(TUNEL)-positive cells in the rhEPO-treated rat brains was far fewer than in the vehicle-treated rat brains. Conclusions: Epo exerts neuroprotective effect against traumatic brain injury via reducing Bax gene expression involved in inhibiting TBI-induced neuronal cell death.
- Subjects
BRAIN injuries; ERYTHROPOIETIN; APOPTOSIS; POLYMERASE chain reaction; LABORATORY mice; GENETICS
- Publication
Neurology India, 2009, Vol 57, Issue 6, p722
- ISSN
0028-3886
- Publication type
Article
- DOI
10.4103/0028-3886.59466