Protective effect of erythropoietin on rats with hypoxic-ischemic brain injury and its mechanism

ZHANG Jing; HUANG Rui; HAO Ling; LIU Na

doi:10.3969/j.issn.1002-266X.2015.17.005

Abstract：Objective To observe the protective effect of erythropoietin (EPO) on rats with hypoxic-ischemic brain injury (HIBD) and to explore its mechanism.Methods A total of 120 Wistar rats in 7-day-old were selected and randomly divided into three groups (n=40):sham operation group (control group), HIBD group and EPO treatment group.After HIBD model was established, EPO (5 000 IU/kg) was injected into rats of the EPO treatment group;while in the HIBD group, the equal vol-ume normal saline was injected.Rats were killed at 6, 12, 24, 48 and 72 h, 8 rats at each time point per group.Then the ex-pression levels of Fas/FasL mRNA and protein in the brain tissues were detected by real-time PCR and Western blotting, respec-tively.Results In HIBD group, Fas mRNA expression was observed at 6 h, increased rapidly and reached the peak at 12 h, then decreased after 24 h;in EPO treatment group, the expression of Fas mRNA was lower than that in HIBD group at each time point, and the difference was significant at time points of 12, 24 and 48 h (all P<0.05).Similarly, FasL mRNA was increased obviously from 6 h to 24 h, and reached the peak at 24 h, and then decreased gradually, the FasL mRNA level was significantly decreased in EPO treatment group as compared with that of the HIBD group at 6, 12, 24 and 48 h (all P<0.05).On the protein level, the Fas and FasL in the control group was very low;and there was a changing trend in the HIBD group , which rose first and then fell;the Fas protein expression at 24 and 48 h, and FasL protein expression at all the time points in the EPO treatment group was significantly decreased (all P<0.05).Conclusion EPO could alleviate the damage of HIBD on neurons in the brain tissue and have an effective protective effect , whose mechanism might be that the apoptosis of neuronal cells are inhibited through the down-regulation of Fas/FasL signal pathway in the HIBD brain tissues.