Effect of erythropoietin on mitochondrial biogenesis in cardiomyocytes during chronic hypoxia in vitro

周胜凯; 秦川; 陈林; 肖颖彬

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Effect of erythropoietin on mitochondrial biogenesis in cardiomyocytes during chronic hypoxia in vitro

更新时间：2026-01-09

- Effect of erythropoietin on mitochondrial biogenesis in cardiomyocytes during chronic hypoxia in vitro
- Journal of Army Medical University Vol. 35, Issue 12, Pages: 1192-1196(2013)
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  CLC： R322.11;R329.26;R364.4
- Published：2013
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周胜凯,秦川,陈林,肖颖彬.EPO对慢性缺氧心肌细胞线粒体生物合成的影响[J].陆军军医大学学报(原第三军医大学学报),2013,35(12):1192-1196.

　Zhou Shengkai,Qin Chuan,Chen Lin,Xiao Yingbin.Effect of erythropoietin on mitochondrial biogenesis in cardiomyocytes during chronic hypoxia in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(12):1192-1196.
周胜凯,秦川,陈林,肖颖彬.EPO对慢性缺氧心肌细胞线粒体生物合成的影响[J].陆军军医大学学报(原第三军医大学学报),2013,35(12):1192-1196. DOI：

　Zhou Shengkai,Qin Chuan,Chen Lin,Xiao Yingbin.Effect of erythropoietin on mitochondrial biogenesis in cardiomyocytes during chronic hypoxia in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(12):1192-1196. DOI：

摘要

目的观察促红细胞生成素（erythropoietin

EPO）在慢性缺氧条件下对心肌线粒体生物合成的影响及其可能的机制。方法将H9c2心肌细胞株置入缺氧培养箱7 d（94% N

，5%CO

，1%O

），建立H9c2心肌细胞株慢性缺氧模型；采用5、10、20 U/mL不同浓度的rhEPO（recombinant human erythropoietin；重组人促红细胞生成素）干预处理后，用荧光探针标记线粒体，观察线粒体数目的变化；RT-PCR技术检测线粒体DNA的相对拷贝数变化；Western blot技术检测Akt、eNOS及其磷酸化蛋白水平的变化。结果 rhEPO干预7 d后线粒体数目及拷贝数增加（

0.05）；Akt、eNOS蛋白磷酸化水平增强（

0.05），Akt、eNOS总蛋白无明显变化（

0.05）。结论 EPO增强了慢性缺氧心肌细胞的线粒体生物合成，Akt、eNOS可能是EPO增强线粒体生物合成的重要信号通路。

Abstract

Objective To determine the effect of erythropoietin (EPO) on the mitochondrial biogenesis in rat cardiomyocytes under the condition of chronic hypoxia. Methods Rat cardiomyocyte-derived H9c2 cells were deprived of oxygen for 7 d to establish the chronic hypoxia model (94% N

5%CO

and 1%O

). Then the obtained H9c2 cells were treated by recombinant human EPO (rhEPO

10 and 20 U/ml) for 3 or 7 d. Fluorescent probe was used to mark mitochondria in the cells for the amount of mitochondria. The protein levels of Akt

phospho-A

kt (serine473)

endothelial nitric oxide synthase (eNOS)

and phospho-eNOS (serine1177) were determined with Western blotting. RT-PCR was used to detect the relative copy number of mitochondrial DNA. Results rhEPO treatment for 7 d resulted in a significant increase in the amount and copy number of mitochondria (

0.05). The phosphorylation levels of Akt and eNOS were also enhanced

but those of akt and eNOS had no change (

0.05）. Conclusion EPO improves mitochondrial biogenesis in the cardiomyocytes exposure to chronic hypoxia

probably through Akt and eNOS signal transduction.

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