We are analyzing https://link.springer.com/article/10.1186/1423-0127-18-69.

Title:
Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats | Journal of Biomedical Science
Description:
Background Perinatal brain injury is the leading cause of subsequent neurological disability in both term and preterm baby. Glutamate excitotoxicity is one of the major factors involved in perinatal hypoxic-ischemic encephalopathy (HIE). Glutamate transporter GLT1, expressed mainly in mature astrocytes, is the major glutamate transporter in the brain. HIE induced excessive glutamate release which is not reuptaked by immature astrocytes may induce neuronal damage. Compounds, such as ceftriaxone, that enhance the expression of GLT1 may exert neuroprotective effect in HIE. Methods We used a neonatal rat model of HIE by unilateral ligation of carotid artery and subsequent exposure to 8% oxygen for 2 hrs on postnatal day 7 (P7) rats. Neonatal rats were administered three dosages of an antibiotic, ceftriaxone, 48 hrs prior to experimental HIE. Neurobehavioral tests of treated rats were assessed. Brain sections from P14 rats were examined with Nissl and immunohistochemical stain, and TUNEL assay. GLT1 protein expression was evaluated by Western blot and immunohistochemistry. Results Pre-treatment with 200 mg/kg ceftriaxone significantly reduced the brain injury scores and apoptotic cells in the hippocampus, restored myelination in the external capsule of P14 rats, and improved the hypoxia-ischemia induced learning and memory deficit of P23-24 rats. GLT1 expression was observed in the cortical neurons of ceftriaxone treated rats. Conclusion These results suggest that pre-treatment of infants at risk for HIE with ceftriaxone may reduce subsequent brain injury.
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Keywords {🔍}

ceftriaxone, brain, pubmed, glt, article, google, scholar, rats, rat, glutamate, neonatal, expression, cas, injury, figure, saline, hypoxicischemic, pretreatment, hie, protein, transporter, group, test, damage, mgkg, model, avoidance, human, eaat, cell, mbp, neuronal, astrocytes, hrs, sections, hippocampus, observed, treatment, animal, study, animals, cerebral, authors, induced, dosages, reduced, white, matter, board, hippocampal,

Topics {✒️}

neonatal hypoxic-ischemic injury perinatal hypoxic-ischemic encephalopathy hypoxic-ischemic brain injury ischemic-hypoxic brain damage hypoxic-ischemic brain damage strain-related brain injury severe hypoxic-ischemic insults white matter injury hypoxia-ischemia induced learning neonatal hypoxic-ischemic rats beta-lactam antibiotic neonatal cerebral hypoxia-ischemia developing white matter yen ta huang & ted white matter vulnerability biomedical science aims open access article hypoxic-ischemic injury hypoxic-ischemic damage hypoxic-ischemic encephalopathy long-term pharmacologic neuroprotection article download pdf brain injury score dose-dependently attenuated transient forebrain ischemia ching-jung lai ischemic-hypoxic side negative geotaxis test brain injury scores left carotid artery delayed neuronal damage related subjects excitatory amino acids ceftriaxone significantly reduced yen ta huang ischemic-hypoxic insult reduce neurological damage cliff avoidance test chia chen wu brain damage caused ceftriaxone significantly attenuated privacy choices/manage cookies protein extraction solution article lai induce neuronal damage authors’ original file betulinic acid hydroxamate tzu chi university considered statistically significant hypoxia-ischemia challenge

Questions {❓}

Van Bel F, Groenendaal F: Long-term pharmacologic neuroprotection after birth asphyxia: where do we stand?

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         headline:Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats
         description:Perinatal brain injury is the leading cause of subsequent neurological disability in both term and preterm baby. Glutamate excitotoxicity is one of the major factors involved in perinatal hypoxic-ischemic encephalopathy (HIE). Glutamate transporter GLT1, expressed mainly in mature astrocytes, is the major glutamate transporter in the brain. HIE induced excessive glutamate release which is not reuptaked by immature astrocytes may induce neuronal damage. Compounds, such as ceftriaxone, that enhance the expression of GLT1 may exert neuroprotective effect in HIE. We used a neonatal rat model of HIE by unilateral ligation of carotid artery and subsequent exposure to 8% oxygen for 2 hrs on postnatal day 7 (P7) rats. Neonatal rats were administered three dosages of an antibiotic, ceftriaxone, 48 hrs prior to experimental HIE. Neurobehavioral tests of treated rats were assessed. Brain sections from P14 rats were examined with Nissl and immunohistochemical stain, and TUNEL assay. GLT1 protein expression was evaluated by Western blot and immunohistochemistry. Pre-treatment with 200 mg/kg ceftriaxone significantly reduced the brain injury scores and apoptotic cells in the hippocampus, restored myelination in the external capsule of P14 rats, and improved the hypoxia-ischemia induced learning and memory deficit of P23-24 rats. GLT1 expression was observed in the cortical neurons of ceftriaxone treated rats. These results suggest that pre-treatment of infants at risk for HIE with ceftriaxone may reduce subsequent brain injury.
         datePublished:2011-09-21T00:00:00Z
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      headline:Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats
      description:Perinatal brain injury is the leading cause of subsequent neurological disability in both term and preterm baby. Glutamate excitotoxicity is one of the major factors involved in perinatal hypoxic-ischemic encephalopathy (HIE). Glutamate transporter GLT1, expressed mainly in mature astrocytes, is the major glutamate transporter in the brain. HIE induced excessive glutamate release which is not reuptaked by immature astrocytes may induce neuronal damage. Compounds, such as ceftriaxone, that enhance the expression of GLT1 may exert neuroprotective effect in HIE. We used a neonatal rat model of HIE by unilateral ligation of carotid artery and subsequent exposure to 8% oxygen for 2 hrs on postnatal day 7 (P7) rats. Neonatal rats were administered three dosages of an antibiotic, ceftriaxone, 48 hrs prior to experimental HIE. Neurobehavioral tests of treated rats were assessed. Brain sections from P14 rats were examined with Nissl and immunohistochemical stain, and TUNEL assay. GLT1 protein expression was evaluated by Western blot and immunohistochemistry. Pre-treatment with 200 mg/kg ceftriaxone significantly reduced the brain injury scores and apoptotic cells in the hippocampus, restored myelination in the external capsule of P14 rats, and improved the hypoxia-ischemia induced learning and memory deficit of P23-24 rats. GLT1 expression was observed in the cortical neurons of ceftriaxone treated rats. These results suggest that pre-treatment of infants at risk for HIE with ceftriaxone may reduce subsequent brain injury.
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      name:Department of Research, Buddhist Tzu Chi General Hospital, Hualien, Taiwan
      name:Department of Physiology, Tzu Chi University, Hualien, Taiwan
      name:Department of Pediatrics, Buddhist Tzu Chi General Hospital, Hualien, Taiwan
      name:Institute of Pharmacology and Toxicology, Tzu Chi University, Hualien, Taiwan
      name:Department of Pharmacology, Tzu Chi University, Hualien, Taiwan

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