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 ORIGINAL ARTICLE
Year : 2009  |  Volume : 57  |  Issue : 6  |  Page : 722--728

Erythropoietin can promote survival of cerebral cells by downregulating Bax gene after traumatic brain injury in rats


1 Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing - 400 016, China
2 Medical Laboratory, Chongqing Medical University, Chongqing - 400 016, China

Correspondence Address:
Z B Liao
Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing- 400 016
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.59466

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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.






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