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| Research on neuroprotective mechanism of EPO in hypoxic environment |
| LAN Haixia1 CHUN Ying1 HU Gejile2▲ |
1.Department of Paediatrics, the 969th Hospital of the People′s Liberation Army, Inner Mongolia Autonomous Region, Hohhot 010051, China;
2.Department of Clinical Laboratory, the Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia Autonomous Region, Hohhot 010059, China |
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Abstract Objective To discuss the effect of erythropoietin (EPO) on the proliferation of U251 cells and the levels of BMI1 gene transcription in hypoxia environment of cobalt chloride (CoCl2), and lay the foundation for studying the role of EPO on neuroprotection. Methods The experimental cells were divided into control group (0 μmol/mL CoCl2), CoCl2 group (400 μmol/mL CoCl2) and CoCl2+EPO group (400 μmol/mL CoCl2 and 75 U/mL EPO). The hypoxia model was evaluated by measuring the effect of CoCl2 on cell proliferation by CCK-8 method; the effect of EPO on the proliferation of U251 cells was detected by CCK-8 method; the changes of BMI1 gene transcription levels in CoCl2 group and CoCl2+EPO group was detected by qPCR method. Results The cell proliferation levels in the CoCl2 group at 48 h were lower than those in the control group, and the differences were statistically significant (P ＜ 0.05); the proliferation levels in the CoCl2+EPO group were higher than those in the CoCl2 group, with a statistically significant differences (P ＜ 0.05). The levels of transcription of BMI1 gene in CoCl2+EPO group were higher than those in CoCl2 group, and the differences were statistically significant (P ＜ 0.05). Conclusion This study successfully constructed a hypoxia model of human glial U251 cells with CoCl2. EPO promotes U251 cell proliferation by up-regulating the expression of the BMI1 gene under hypoxic conditions, and EPO has a protective effect on nerve cells.
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