Effects of Hypothermia and Allopurinol on Oxidative Status in a Rat Model of Hypoxic Ischemic Encephalopathy

Hypoxic ischemic encephalopathy (HIE) is one of the main causes of morbidity and mortality during the neonatal period, despite treatment with hypothermia. There is evidence that oxidative damage plays an important role in the pathophysiology of hypoxic-ischemic (HI) brain injury. Our aim was to inve...

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Bibliographic Details
Published in:Antioxidants 2021-09, Vol.10 (10), p.1523
Main Authors: Durán Fernández-Feijóo, Cristina, Rodríguez-Fanjul, Javier, Lopez-Abat, Miriam, Hadley, Stephanie, Cavia-Saiz, Mónica, Muñiz, Pilar, Arnaez, Juan, Fernández-Lorenzo, José Ramón, Camprubí Camprubí, Marta
Format: Article
Language:English
Subjects:
Allopurinol
Animal models
Antioxidants
Biomarkers
Brain injury
Carotid arteries
Cerebrospinal fluid
Encephalopathy
Free radicals
Hypothermia
Hypoxia
hypoxic-ischemic encephalopathy
Ischemia
Juveniles
Laboratory animals
Lipid peroxidation
Morbidity
Neonates
Neuroprotection
oxidative damage
Oxidative stress
Plasma
Proteins
Sulfonic acid
Traumatic brain injury
Veins & arteries
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Summary:Hypoxic ischemic encephalopathy (HIE) is one of the main causes of morbidity and mortality during the neonatal period, despite treatment with hypothermia. There is evidence that oxidative damage plays an important role in the pathophysiology of hypoxic-ischemic (HI) brain injury. Our aim was to investigate whether postnatal allopurinol administration in combination with hypothermia would reduce oxidative stress (OS) biomarkers in an animal model of HIE. Postnatal 10-day rat pups underwent unilateral HI of moderate severity. Pups were randomized into: Sham operated, hypoxic-ischemic (HI), HI + allopurinol (HIA), HI + hypothermia (HIH), and HI + hypothermia + allopurinol (HIHA). Biomarkers of OS and antioxidants were evaluated: GSH/GSSG ratio and carbonyl groups were tested in plasma. Total antioxidant capacity (TAC) was analyzed in plasma and cerebrospinal fluid, and 8-iso-prostaglandin F2α was measured in brain tissue. Plasma 2,2′–azinobis-(3-ethyl-benzothiazoline-6-sulfonic acid) (ABTS) levels were preserved in those groups that received allopurinol and dual therapy. In cerebrospinal fluid, only the HIA group presented normal ferric reducing ability of plasma (FRAP) levels. Protein oxidation and lipid peroxidation were significantly reduced in all groups treated with hypothermia and allopurinol, thus enhancing neuroprotection in HIE.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox10101523