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

ZB Liao, GY Jiang, ZH Tang, XG Zhi, XC Sun, WY Tang, MJ Wu
2009 Neurology India  
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
more » ... istar 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.
doi:10.4103/0028-3886.59466 pmid:20139499 fatcat:abiseecierdezckqctxwd563ia