[Effects of recombinant human erythropoietin on brain-derived neurotrophic factor expression in different brain regions of aging rats].
Autor: | Wang HQ; Department of Neurology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China. E-mail: tigerwhq@sohu.com., Gao Z, Chen MY, Wu HQ, Zhang GL, Zhan SQ, Bu N, Liu JJ, Zhai YF |
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Jazyk: | čínština |
Zdroj: | Nan fang yi ke da xue xue bao = Journal of Southern Medical University [Nan Fang Yi Ke Da Xue Xue Bao] 2016 Apr 20; Vol. 37 (4), pp. 551-554. |
Abstrakt: | Objective: To explore the effect of recombinant human erythropoietin (rhEPO) on expression of brain-derived neurotrophic factor (BDNF) in different brain regions of aging rats. Methods: Forty male SD rats were randomized equally into negative control group, D-galactose group, EPO treatment group, and positive control group. Rat models of subacute aging were established by continuous subcutaneous injection of 5% D-galactose. Immunohistochemical staining was used to analyze the variation of BDNF expressions in different brain regions of the aging rats with different treatments. Results: Significant brain region-specific differences in BDNF expression were found among the rats in different groups. Compared with those in the negative control group, the numbers of BDNF-positive cells in the hippocampal CA1 region, CA3 region, dentate gyrus (DG) and frontal cortex were all decreased obviously in D-galactose group (P<0.05) but increased in both EPO group and the positive control group (P<0.05) without significant differences between the latter two groups. In the rats in the same group, the number of BDNF-positive cells varied markedly in different brain regions (P<0.05), and the expression level of BDNF was the highest in the frontal cortex followed by the hippocampal CA3 region and the dentate gyrus, and was the lowest in the hippocampal CA1 region. Conclusion: Treatment with rhEPO enhances the expression of BDNF in rat neural cells, suggesting that rhEPO may protect the nervous system from aging by regulating the BDNF pathway. |
Databáze: | MEDLINE |
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