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Erythropoietin can promote survival of cerebral cells by downregulating Bax gene after traumatic brain injury in rats.
Neurol India. 2009 Nov-Dec; 57(6):722-8.NI

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.

Authors+Show Affiliations

Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. liaozhengbu@hotmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20139499

Citation

Liao, Z B., et al. "Erythropoietin Can Promote Survival of Cerebral Cells By Downregulating Bax Gene After Traumatic Brain Injury in Rats." Neurology India, vol. 57, no. 6, 2009, pp. 722-8.
Liao ZB, Jiang GY, Tang ZH, et al. Erythropoietin can promote survival of cerebral cells by downregulating Bax gene after traumatic brain injury in rats. Neurol India. 2009;57(6):722-8.
Liao, Z. B., Jiang, G. Y., Tang, Z. H., Zhi, X. G., Sun, X. C., Tang, W. Y., & Wu, M. J. (2009). Erythropoietin can promote survival of cerebral cells by downregulating Bax gene after traumatic brain injury in rats. Neurology India, 57(6), 722-8. https://doi.org/10.4103/0028-3886.59466
Liao ZB, et al. Erythropoietin Can Promote Survival of Cerebral Cells By Downregulating Bax Gene After Traumatic Brain Injury in Rats. Neurol India. 2009 Nov-Dec;57(6):722-8. PubMed PMID: 20139499.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Erythropoietin can promote survival of cerebral cells by downregulating Bax gene after traumatic brain injury in rats. AU - Liao,Z B, AU - Jiang,G Y, AU - Tang,Z H, AU - Zhi,X G, AU - Sun,X C, AU - Tang,W Y, AU - Wu,M J, PY - 2010/2/9/entrez PY - 2010/2/9/pubmed PY - 2010/4/23/medline SP - 722 EP - 8 JF - Neurology India JO - Neurol India VL - 57 IS - 6 N2 - 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. SN - 0028-3886 UR - https://www.unboundmedicine.com/medline/citation/20139499/Erythropoietin_can_promote_survival_of_cerebral_cells_by_downregulating_Bax_gene_after_traumatic_brain_injury_in_rats_ L2 - http://www.neurologyindia.com/article.asp?issn=0028-3886;year=2009;volume=57;issue=6;spage=722;epage=728;aulast=Liao DB - PRIME DP - Unbound Medicine ER -