Carbamylated erythropoietin attenuates cardiomyopathy via PI3K/Akt activation in rats with diabetic cardiomyopathy

  • Authors:
    • Hongying He
    • Xiaoyu Qiao
    • Suisheng Wu
  • View Affiliations

  • Published online on: May 31, 2013     https://doi.org/10.3892/etm.2013.1134
  • Pages: 567-573
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Abstract

The aim of the present study was to investigate the protective effect of carbamylated erythropoietin (CEPO) against cardiomyopathy in high‑fat, high‑carbohydrate diet‑fed rats with streptozotocin (STZ)‑induced diabetic cardiomyopathy (DCM). Healthy male Wistar rats were fed a high‑fat, high‑carbohydrate diet for four weeks, and then were injected with STZ twice (50 mg/kg, intraperitoneally). Once DCM was confirmed, the rats were divided randomly into the following groups: DCM without treatment, CEPO treatment at different dosages (500, 1,000 or 2,000 IU/kg) or recombinant human erythropoietin (rhEPO) treatment (1,000 IU/kg), for a four‑week short intervention or an eight-week long intervention protocol. Healthy rats were used as normal controls. Venous blood samples were drawn for routine hematological examinations, and heart tissues were collected for histological analysis, as well as the determination of myocardial apoptosis and phosphatidylinositol‑3‑kinase (PI3K)/Akt signaling. CEPO treatment had no significant effect on the erythrocyte or hemoglobin levels in the rats with DCM; however, it reduced myocardial cell apoptosis in the rats and protected the cellular ultrastructure. In addition, CEPO treatment inhibited caspase‑3 and increased Bcl‑xl protein expression (P<0.05). It also increased PI3K (p85) and Akt1 expression at the mRNA and protein levels in the hearts of the rats with DCM, with a dose‑response relationship. An eight‑week treatment using CEPO, in comparison with a four‑week protocol, marginally increased PI3K (p85) and Akt1 expression, and did not demonstrate significant benefit. The study indicated that CEPO protects against DCM, without markedly affecting erythropoiesis, and that the activation of PI3K/Akt may be a key mechanism in the protection conferred by CEPO.
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August 2013
Volume 6 Issue 2

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
He H, Qiao X and Wu S: Carbamylated erythropoietin attenuates cardiomyopathy via PI3K/Akt activation in rats with diabetic cardiomyopathy. Exp Ther Med 6: 567-573, 2013
APA
He, H., Qiao, X., & Wu, S. (2013). Carbamylated erythropoietin attenuates cardiomyopathy via PI3K/Akt activation in rats with diabetic cardiomyopathy. Experimental and Therapeutic Medicine, 6, 567-573. https://doi.org/10.3892/etm.2013.1134
MLA
He, H., Qiao, X., Wu, S."Carbamylated erythropoietin attenuates cardiomyopathy via PI3K/Akt activation in rats with diabetic cardiomyopathy". Experimental and Therapeutic Medicine 6.2 (2013): 567-573.
Chicago
He, H., Qiao, X., Wu, S."Carbamylated erythropoietin attenuates cardiomyopathy via PI3K/Akt activation in rats with diabetic cardiomyopathy". Experimental and Therapeutic Medicine 6, no. 2 (2013): 567-573. https://doi.org/10.3892/etm.2013.1134