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Updated: Feb 23, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

The Immunoreactivity of PI3K/AKT Pathway After Prenatal Hypoxic Damage

Huisun Wang¹, Yoonyoung Chung², Sun-Kyoung Yu³

¹Department of Neurosurgery, Chosun University Hospital, Gwang-ju, Republic of Korea.

In Vivo (Athens, Greece)

|September 9, 2017

Abstract

Background/Aim:

There is no consensus on the effect of hypoxia on neurogenesis. In this study, we investigated the immunoreactivity of BDNF and PI3K/Akt signaling after uterine artery ligation in pregnant rats.

Materials And Methods:

Unilateral uterine artery ligation was performed at 16 days of gestation (dg). Fetuses from one horn with ligated artery were allocated to the hypoxic group. Immunohistochemistry was performed with primary antibodies; NeuN, BDNF, PI3K, Akt and phospho-Akt (pAkt).

Results:

The densities of NeuN- and BDNF-immunoreactive (IR) cells in the cerebral cortex were lower in the hypoxic fetuses than in the controls at 21 dg. The density of PI3K and pAkt-IR cells in the cortex of the hypoxic group significantly decreased. The results in dentate gyrus were similar to the results in the cerebral cortex.

Conclusion:

Prenatal hypoxia reduced Akt phosphorylation, which affected neuronal survival in the cortex and dentate gyrus.

Keywords:

Akt PI3K Prenatal hypoxia neurogenesis pAkt

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