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.
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 humanEPO 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.
Authors: Ramon Diaz-Arrastia; Patrick M Kochanek; Peter Bergold; Kimbra Kenney; Christine E Marx; Col Jamie B Grimes; L T C Yince Loh; L T C Gina E Adam; Devon Oskvig; Kenneth C Curley; Wanda Salzer Journal: J Neurotrauma Date: 2014-01-15 Impact factor: 5.269
Authors: Michelle E Schober; Daniela F Requena; Benjamin Block; Lizeth J Davis; Christopher Rodesch; T Charles Casper; Sandra E Juul; Raymond P Kesner; Robert H Lane Journal: J Neurotrauma Date: 2014-02-15 Impact factor: 5.269
Authors: Jovany Cruz Navarro; Shibu Pillai; Lucido L Ponce; Mai Van; Jerry Clay Goodman; Claudia S Robertson Journal: Front Immunol Date: 2014-10-09 Impact factor: 7.561