NDLI: Treatment with harmine ameliorates functional impairment and neuronal death following traumatic brain injury.

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Treatment with harmine ameliorates functional impairment and neuronal death following traumatic brain injury.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhong, Zeqi Tao, Yuan Yang, Hui
Description	Author Affiliation: Zhong Z ( Department of Neurosurgery, Xinqiao Hospital, The Third Military Medical University, Chongqing 400037, P.R. China.); Tao Y ( Department of Neurology, Research Institute of Field Surgery, Daping Hospital, The Third Military Medical University, Chongqing 400042, P.R. China.); Yang H ( Department of Neurosurgery, Xinqiao Hospital, The Third Military Medical University, Chongqing 400037, P.R. China.)
Abstract	Traumatic brain injury (TBI) is a leading cause of mortality in young individuals, and results in motor and cognitive deficiency. Excitotoxicity is an important process during neuronal cell death, which is caused by excessive release of glutamate following TBI. Astrocytic glutamate transporters have a predominant role in maintaining extracellular glutamate concentrations below excitotoxic levels, and glutamate transporter 1 (GLT1) may account for >90% of glutamate uptake in the brain. The ßcarboline alkaloid harmine has been demonstrated to exert neuroprotective actions in vivo, and the beneficial effects were specifically due to elevation of GLT1. However, whether harmine provides neuroprotection following TBI remains to be elucidated. The present study performed intraperitoneal harmine injections in rats (30 mg/kg per day for up to 5 days), in order to investigate whether harmine treatment attenuates brain edema and improves functional recovery in a rat model of TBI. The neuronal survival ratio and the protein expression of apoptosisassociated caspase 3 were also assessed in the hippocampus of the rat brain. Furthermore, the expression levels of GLT1 and inflammatory cytokines were detected, in order to determine the underlying mechanisms. The results of the present study demonstrated that administration of harmine significantly attenuated cerebral edema, and improved learning and memory ability. In addition, harmine significantly increased the protein expression of GLT1, and markedly attenuated the expression levels of interleukin1ß and tumor necrosis factor , thereby attenuating apoptotic neuronal death in the hippocampus. These results provided in vivo evidence that harmine may exert neuroprotective effects by synergistically reducing excitotoxicity and inflammation following TBI.
ISSN	17912997
e-ISSN	17913004
DOI	10.3892/mmr.2015.4437
Journal	Molecular Medicine Reports
Issue Number	6
Volume Number	12
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-12-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Apoptosis Drug Effects Harmine Pharmacology Neurons Neuroprotective Agents Animals Brain Edema Drug Therapy Etiology Metabolism Brain Injuries Pathology Caspase 3 Disease Models, Animal Excitatory Amino Acid Transporter 2 Therapeutic Use Hippocampus Interleukin-1beta Maze Learning Microscopy, Fluorescence Rats, Sprague-dawley Spatial Memory Tumor Necrosis Factor-alpha Up-regulation Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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