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Biological Research

Print version ISSN 0716-9760

Abstract

DIAO, Min et al. Effect of carbamylated erythropoietin on neuronal apoptosis in fetal rats during intrauterine hypoxic‑ischemic encephalopathy. Biol. Res. [online]. 2019, vol.52, 28.  Epub June 13, 2019. ISSN 0716-9760.  http://dx.doi.org/10.1186/s40659-019-0234-7.

Background:

Hypoxic-ischemic encephalopathy (HIE) is a common disease that occurs during the perinatal period. The primary cause of neonatal HIE is related to fetal intrauterine anoxia. Carbamylated erythropoietin (CEPO), a derivative of erythropoietin (EPO), does not exert any erythropoietic effect; however, the neuroprotective effects resemble those of EPO. Previous studies have shown the potential benefits of CEPO on the central nervous system. The present study aimed to investigate the role of CEPO in neuronal apoptosis during intrauterine HIE and the underlying mechanisms.

Results:

To validate our hypothesis, we established an intrauterine HIE model by occluding the bilateral uteroovarian arteries of pregnant Sprague–Dawley rats. Compared to the I/R group, neuronal apoptosis in the CEPO group was significantly lower at 4, 12, 24, and 48 h (P < 0.05). CEPO significantly inhibited CC3 expression (P < 0.05) during the early-stages after ischemia–reperfusion (0.5, 4, 8, 12 and 24 h), upregulated Bcl-2 expression, and downregulated Bax expression at 4, 8, 12, and 24 h (P < 0.05).

Conclusions:

Carbamylated erythropoietin pretreatment inhibited the expression of proapoptotic protein CC3 in brain and regulated the Bcl-2/Bax ratio, resulting in reduced neuronal apoptosis and thus resulting in a protective effect on intrauterine HIE.

Keywords : Carbamylated erythropoietin; Neuronal apoptosis; Intrauterine hypoxic-ischemic encephalopathy.

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