Background: Hypoxic-ischemic brain injury (HIBI) is a common cause of neonatal mortality and morbidity. The use of levetiracetam (LEV), as a potential neuroprotective in brain ischemia, receives an increasingly high attention, and it could have a crucial role in the regulation of epileptogenesis and neuroprotection. Potential effects of LEV on neuronal apoptosis in HIBI have not previously been reported in literature.
Objectives: The aim of this study is to evaluate the possible effects of LEV on neuronal apoptosis in neonatal rat model of HIBI.
Methods: Seven-day-old Wistar rat pups were subjected to right common carotid artery ligation and hypoxia (92% nitrogen and 8% oxygen) for 2h. The pups were treated with LEV or saline after hypoxia. In sham group rats, neither ligation, nor hypoxia was performed. Neuronal apoptosis was evaluated by the terminal deoxynucleotidyl-transferase- mediated dUTP nick-end labeling (TUNEL) methods.
Results: The counts of apoptotic cells in both hippocampus and cerebral cortex were significantly higher in the saline treatment group than in the sham group. The counts of apoptotic cells in both hippocampus and cerebral cortex were similar to those in the sham group and in the LEV treatment group. The number of apoptotic cells decreased significantly in the LEV-treated group compared with the saline group.
Conclusions: These results show that LEV administration after hypoxia reduces neuronal apoptosis. Thus, we propose that LEV, as an effective antiepileptic and antiapoptotic drug, may be a viable choice for the control of seizure activity in neonates with HIBI.
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http://dx.doi.org/10.1016/j.earlhumdev.2012.12.002 | DOI Listing |
Adv Healthc Mater
January 2025
Department of Otorhinolaryngology-Head and Neck Surgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, P. R. China.
Noise-induced hearing loss (NIHL) results from prolonged exposure to intense noise, causing damage to sensory outer hair cells (OHCs) and spiral ganglion neurons (SGNs). The blood labyrinth barrier (BLB) hinders systemic drug delivery to the inner ear. This study applied a retro-auricular round window membrane (RWM) method to bypass the BLB, enabling the transport of macromolecular proteins into the inner ear.
View Article and Find Full Text PDFBrain Res
January 2025
Neuropharmacology Division, Department of Pharmacology, ISF College of Pharmacy, Moga 142001, Punjab, India. Electronic address:
Neurodegenerative disorders are characterized by a progressive loss of neurons, causing substantial deficits in motor and cognitive functioning. Bilirubin is a yellow by-product of heme, existing in two primary isoforms namely unconjugated and conjugated, while initially produced unconjugated isomer is lipophilic and cytotoxic in nature. At physiological levels, bilirubin has an important role in brain function by acting as a powerful antioxidant, preventing brain tissues from oxidative damage by eliminating reactive oxygen species (ROS).
View Article and Find Full Text PDFSci Rep
January 2025
Neuroscience and Ophthalmology, Department of Inflammation and Ageing, School of Infection, Inflammation and Immunology, College of Medicine and Health, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.
Spinal cord injury (SCI) is a significant cause of lifelong disability, with no available disease-modifying treatments to promote neuroprotection and axon regeneration after injury. Photobiomodulation (PBM) is a promising therapy which has proven effective at restoring lost function after SCI in pre-clinical models. However, the precise mechanism of action is yet to be determined.
View Article and Find Full Text PDFCell Rep
January 2025
Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA; The Brain Tumor Center, Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
Mutation or deletion of the deubiquitinase USP7 causes Hao-Fountain syndrome (HAFOUS), which is characterized by speech delay, intellectual disability, and aggressive behavior and highlights important unknown roles of USP7 in the nervous system. Here, we conditionally delete USP7 in glutamatergic neurons in the mouse forebrain, triggering disease-relevant phenotypes, including sensorimotor deficits, impaired cognition, and aggressive behavior. Although USP7 deletion induces p53-dependent neuronal apoptosis, most behavioral abnormalities in USP7 conditional knockout mice persist following p53 loss.
View Article and Find Full Text PDFPlants (Basel)
January 2025
Faculty of Pharmaceutical Sciences, Khon Kaen University, Khon Kaen 40002, Thailand.
Alzheimer's disease (AD) is a neurodegenerative condition characterized by a gradual decline in cognitive function, for which few effective treatments exist. This study investigated the neuroprotective potential of root extract and its key constituents (baicalein, chrysin, oroxylin A) against AD hallmarks. The extract and its constituents exhibited antioxidant activity in the DPPH assay.
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