Corticosteroid responses following hypoxic preconditioning provide neuroprotection against subsequent hypoxic-ischemic brain injury in the newborn rats |
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| Institution: | 1. Department of Children’s and Adolescent Health, Public Health College of Harbin Medical University, Harbin 150081, China;2. Department of Nursing, Daqing Campus of Harbin Medical University, Daqing 163319, China;3. Department of Pediatric, the Second Affiliated Hospital of Harbin Medical University, Harbin 150081, China;4. Department of Pharmacology, Daqing Campus of Harbin Medical University, Daqing 163319, China;1. Department of Neurobiology, Institute for Biological Research, University of Belgrade, Bulevar despota Stefana 142, 11060 Belgrade, Serbia;2. Department of Biochemistry and Goodman Cancer Research Centre, McGill University, 1160 Pine Ave. West, H3A 1A3 Montreal, QC, Canada;1. Neuropsychophysiology Laboratory, CIPsi School of Psychology, University of Minho, Braga, Portugal;2. CIPsi School of Psychology, University of Minho, Braga, Portugal;3. Department of Counseling and Applied Educational Psychology, Bouvé College of Health Sciences, Northeastern University, Boston, MA, USA;4. Spaulding Center of Neuromodulation, Department of Physical Medicine & Rehabilitation, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA;1. Department of Pediatrics, Laval University Center de Recherche du Center Hospitalier Universitaire (CHU) de Québec, Hôpital St-François d''Assise, 10 Rue de l''Espinay, Québec, QC G1L 3L5, Canada;2. Institute of Veterinary Physiology, Vetsuisse-Faculty University of Zurich, Winterthurerstrasse 260, CH-8057 Zurich, Switzerland;1. Department of Pediatrics, Faculty of Medicine, Kagawa University, Kagawa, Japan;2. Department of Neonatology, National Hospital Organization Okayama Medical Center, Okayama, Japan;3. Maternal Perinatal Center, Faculty of Medicine, Kagawa University, Kagawa, Japan;4. Departments of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa, Japan;5. Departments of Anatomy and Neurobiology, Faculty of Medicine, Kagawa University, Kagawa, Japan;6. Departments of Perinatology and Gynecology, Faculty of Medicine, Kagawa University, Kagawa, Japan;1. Institute of Clinical Physiology, National Research Council (CNR), via Moruzzi 1, Pisa, Italy;2. Department of Translational Research on New Technologies in Medicine and Surgery, via Roma 55, Pisa, Italy;3. Institute of Biophysics, National Research Council (CNR), via Moruzzi 1, Pisa, Italy |
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| Abstract: | Limited research has evaluated the corticosteroids (CS) response in hypoxic preconditioning (PC) induced neuroprotection against subsequent hypoxic-ischemic (HI) brain injury in newborns. To measure, CS response to hypoxic PC, at postnatal day 6 (P6), rat pups were randomly divided into sham, NoPC (exposure to 21% O2) and PC (exposure to 8% O2 for 3 h) groups. In a separate experiment, at P6, rat pups were randomly divided into three groups (sham, NoPC + HI, PC + HI). Rat pups in NoPC + HI and PC + HI groups, respectively had normoxic or hypoxic exposure for 3 h at P6 and then had the right carotid artery permanently ligated followed by 140 min of hypoxia at P7 (HI). Plasma CS levels were measured at 0.5, 1, 3, 6 and 12 h after hypoxic PC and hypoxic PC followed by HI. To investigate whether CS response to hypoxic PC provides neuroprotection against HI, at P6, rat pups were randomly divided into five groups. Fifteen minutes prior to PC or normoxic exposure, rat pups in DMSO + PC + HI and DMSO + NoPC + HI groups received DMSO while in RU486 + PC + HI and RU486 + NoPC + HI groups received RU486 (glucocorticoid receptor blocker, 60 mg/kg) s.c., respectively. Afterwards, rat pups were exposed to normoxia (DMSO + NoPC + HI, RU486 + NoPC + HI) or hypoxia (DMSO + PC + HI, RU486 + PC + HI) for 3 h and then HI 24 h later (P7). Rat pups at the corresponding age without any exposure to PC or HI or RU486/DMSO were used as sham. We found that hypoxic PC caused CS surge as well as augmented CS surge and preserved the glucocorticoid feedback regulation after HI. Hypoxic PC reduced HI induced early and delayed brain damage. RU486 partially but significantly inhibited hypoxic PC induced neuroprotection. |
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| Keywords: | Glucocorticoids Hypoxic tolerance Neuroprotection CNS injury Newborn rat |
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