ArticleJournal of biomedical science2011
Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats.
Article in Journal of biomedical science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Role of astrocytes in the pathogenesis of perinatal brain injury.Molecular medicine (Cambridge, Mass.) · 2025Review
- Effects of prenatal mobile phone radiation exposure on MMP9 expression: Implications for inflammation, oxidative stress, and sensory-motor impairment after neonatal hypoxia- ischemia in rats.Toxicology reports · 2023Article
- The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation.Frontiers in molecular neuroscience · 2023Review
- Ceftriaxone as a Novel Therapeutic Agent for Hyperglutamatergic States: Bridging the Gap Between Preclinical Results and Clinical Translation.Frontiers in neuroscience · 2022Review
- Evaluating Neuroprotective Effects of Uridine, Erythropoietin, and Therapeutic Hypothermia in a Ferret Model of Inflammation-Sensitized Hypoxic-Ischemic Encephalopathy.International journal of molecular sciences · 2021Article
- Neurobiology, Functions, and Relevance of Excitatory Amino Acid Transporters (EAATs) to Treatment of Refractory Epilepsy.CNS drugs · 2020Review
- Hippocampal and Cerebellar Changes in Acute Restraint Stress and the Impact of Pretreatment with Ceftriaxone.Brain sciences · 2020Article
- Immunomodulatory Mechanism and Potential Therapies for Perinatal Hypoxic-Ischemic Brain Damage.Frontiers in pharmacology · 2020Review
- Ceftriaxone Treatment Affects EAAT2 Expression and Glutamatergic Neurotransmission and Exerts a Weak Anticonvulsant Effect in Young Rats.International journal of molecular sciences · 2019Article
- Distribution and morphology of baroreceptors in the rat carotid sinus as revealed by immunohistochemistry for P2X3 purinoceptors.Histochemistry and cell biology · 2019Article
- Repurposing of the β-Lactam Antibiotic, Ceftriaxone for Neurological Disorders: A Review.Frontiers in neuroscience · 2019Review
- Brain endothelial cells induce astrocytic expression of the glutamate transporter GLT-1 by a Notch-dependent mechanism.Journal of neurochemistry · 2017Article
- Neonatal Dexamethasone Treatment Exacerbates Hypoxia/Ischemia-Induced White Matter Injury.Molecular neurobiology · 2017Article
- Baicalin protects neonatal rat brains against hypoxic-ischemic injury by upregulating glutamate transporter 1Neural regeneration research · 2017Article
- N-Acetylcysteine and Ceftriaxone as Preconditioning Strategies in Focal Brain Ischemia: Influence on Glutamate Transporters Expression.Neurotoxicity research · 2016Article
- Corticostriatal circuitry in regulating diseases characterized by intrusive thinking.Dialogues in clinical neuroscience · 2016Review
- Metabolic Changes Following Perinatal Asphyxia: Role of Astrocytes and Their Interaction with Neurons.Frontiers in aging neuroscience · 2016Review
- Ceftriaxone reverses ketamine-induced lasting EEG and astrocyte alterations in juvenile mice.Drug and alcohol dependence · 2015Article
- Glutamate and GABA imbalance following traumatic brain injury.Current neurology and neuroscience reports · 2015Review
- Neuroprotective effects of ginsenoside Rg1-induced neural stem cell transplantation on hypoxic-ischemic encephalopathy.Neural regeneration research · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPerinatal 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.
methodsWe 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.
resultsPre-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.
conclusionThese results suggest that pre-treatment of infants at risk for HIE with ceftriaxone may reduce subsequent brain injury.
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