Brain to blood efflux as a mechanism underlying the neuroprotection mediated by rapid remote preconditioning in brain ischemia
Autor: | Jana Jachova, Martin Bona, Miroslav Gottlieb, Petra Bonova, Miroslava Nemethova |
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Rok vydání: | 2020 |
Předmět: |
Male
0301 basic medicine Ischemia Glutamic Acid Infarction Brain damage Pharmacology Neuroprotection Brain Ischemia Rats Sprague-Dawley Brain ischemia 03 medical and health sciences 0302 clinical medicine Genetics Animals Medicine Ischemic Preconditioning Molecular Biology Neurons Cell Death business.industry Penumbra Glutamate receptor Brain General Medicine medicine.disease Rats Neuroprotective Agents 030104 developmental biology 030220 oncology & carcinogenesis Ischemic preconditioning medicine.symptom business |
Zdroj: | Molecular Biology Reports. 47:5385-5395 |
ISSN: | 1573-4978 0301-4851 |
Popis: | Glutamate represents the main excitatory neurotransmitter in the mammalian brain; however, its excessive elevation in the extracellular space is cytotoxic and can result in neuronal death. The ischemia initiated brain damage reflects changes in glutamate concentration in peripheral blood. This paper investigated the role of the brain in blood efflux of the glutamate in an improved tolerance of the brain tissue to ischemic conditions. In the rat model of focal brain ischemia, the neuroprotection was initiated by rapid remote ischemic preconditioning (rRIPC). Our results confirmed a strong neuroprotective effect of rRIPC. We observed reduced infarction by about 78% related to improved neuronal survival by about 70% in the ischemic core. The level of tissue glutamate in core and penumbra dropped significantly and decreased to control value also in the core region of the contralateral hemisphere. Despite significant improvement of blood-brain barrier integrity (by about 76%), the additional gain of glutamate content in the peripheral blood was caused by rRIPC. Based on our results, we can assume that neuroprotection mediated by rapid remote ischemic preconditioning could lie in the regulated, whole-brain release of glutamate from nerve tissue to the blood, which preserves neurons from the exposure to glutamate toxicity and results in reduced infarction. |
Databáze: | OpenAIRE |
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