2026-08-23T19:15:06Zhttps://riubu.ubu.es/oai/request

oai:riubu.ubu.es:10259/80692023-11-22T01:05:28Zcom_10259_5827com_10259_5086com_10259_2604col_10259_5828

Durán Fernández-Feijóo, Cristina Rodríguez-Fanjul, Javier López-Abat, Miriam Hadley, Stephanie Cavia Saiz, Mónica Muñiz Rodríguez, Pilar Arnaez, Juan Fernández-Lorenzo, José Ramón Camprubí Camprubí, Marta Allopurinol Hypothermia Hypoxic-ischemic encephalopathy Oxidative stress Oxidative damage 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 2,20–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. 2023-11-21 2023-11-21 2021-09 info:eu-repo/semantics/article http://hdl.handle.net/10259/8069 10.3390/antiox10101523 2076-3921 eng Antioxidants. 2021, V. 10, n. 10, 1523 https://doi.org/10.3390/antiox10101523 http://creativecommons.org/licenses/by/4.0/ info:eu-repo/semantics/openAccess Atribución 4.0 Internacional MDPI