Changes of Oxidative Stress-Related Gene Expression in an in vitro Model of Neonatal Hypoxic-Ischemic Encephalopathy

Dani C.a,b· Pratesi S.Ranieri G.Mannaioni G.b· Gerace E.b

Author affiliations

aDivision of Neonatology, Careggi University Hospital of Florence, Florence, Italy
bDepartment of Neurosciences, Psychology, Drug Research and Child Health, University of Florence, Florence, Italy

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Article / Publication Details

First-Page Preview

Abstract of Original Paper

Received: March 14, 2022
Accepted: July 26, 2022
Published online: September 12, 2022
Issue release date:

Number of Print Pages: 8
Number of Figures: 3
Number of Tables: 0

ISSN: 1661-7800 (Print)
eISSN: 1661-7819 (Online)

For additional information: https://www.karger.com/NEO

Abstract

Background: We recently demonstrated that oxygen-glucose deprivation (OGD) and unconjugated bilirubin (UCB) can damage mature and immature organotypic hippocampal slices and induce an oxidative stress similar to what occurs in jaundiced term and preterm infants with hypoxic-ischemic encephalopathy (HIE). Objectives: To assess the effects of OGD and UCB on the expression of heme-oxygenase 1 (HO-1) and oxidative stress-related enzymes in an in vitro model of HIE. Methods: Mature and immature organotypic hippocampal slices were exposed to 30-min OGD and to 24 h UCB or UCB plus human serum albumin (HSA). The expression of HO-1, superoxide dismutase 1 (SOD1), catalase (CAT), glutathione peroxidase (GPX), and nuclear factor erythroid-related factor 2 were analyzed by real-time PCR. Results: In mature slices, OGD did not affect the expression of HO-1 and oxidative stress-induced enzymes. The addition of UCB was associated with the upregulation of HO-1 and Nrf2 that is abolished by the presence of equimolar amount of HSA. In immature slices, OGD induced the downregulation of CAT, GPX, and Nrf2 expression and the addition of UCB further decreased GPX. The addition of UCB and HSA reverted the effects of OGD and UCB on gene expression. Conclusions: In an in vitro model of HIE in term infants, we did not observe neuroprotective changes of the expression of HO-1 and genes involved in antioxidant defenses. Conversely, in an in vitro model of HIE in preterm infants, we observed a harmful decrease of the expression of genes encoding for antioxidant enzymes.

© 2022 S. Karger AG, Basel

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First-Page Preview

Abstract of Original Paper

Received: March 14, 2022
Accepted: July 26, 2022
Published online: September 12, 2022
Issue release date:

Number of Print Pages: 8
Number of Figures: 3
Number of Tables: 0

ISSN: 1661-7800 (Print)
eISSN: 1661-7819 (Online)

For additional information: https://www.karger.com/NEO

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