ArticlePediatric surgery international2018
Anti-oxidants correct disturbance of redox enzymes in the hearts of rat fetuses with congenital diaphragmatic hernia.
Article in Pediatric surgery international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Alterations of endothelial cell bioenergetics in congenital diaphragmatic hernia.Pediatric research · 2026Article
- EGCG Attenuates CA1 Neuronal Death by Regulating GPx1, NF-κB S536 Phosphorylation and Mitochondrial Dynamics in the Rat Hippocampus following Status Epilepticus.Antioxidants (Basel, Switzerland) · 2023Article
- Physiological Dose of EGCG Attenuates the Health Defects of High Dose by Regulating MEMO-1 inOxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
aimTo evaluate if the redox system is unbalanced in the hearts of nitrofen-induced congenital diaphragmatic hernia (CDH) animals and to study the possible preventive effects of two anti-oxidant treatments, apocynin and epigallocatechin-3-gallate (EGCG).
methodsAdult rats were divided into four groups. Group 1: rats received only vehicle on day E9.5. Group 2: rats received 100 mg nitrofen on day E9.5. Group 3: 1 month before mating rats received apocynin 1.5 mM and, when pregnant, 100 mg nitrofen on day E9.5. Group 4: same than group 3 but with EGCG 30 mg/kg. All fetuses were recovered at term and the hearts were processed. Nox activity and mRNA levels of Nox1, Nox2, Nox4, SOD1, SOD2, SOD3, catalase, and GPX1 were analyzed. Nox, SOD, and Catalase activity and H2O2 production were also evaluated.
resultsNox activity, H
conclusionThese findings suggest a possible preventive effect on the abnormal redox metabolism of anti-oxidant treatments in the hearts from rat fetuses with CDH. If the same occurs in humans, it could represent a potential tool in future prenatal treatment.
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